In the United States Court of Federal Claims

OFFICE OF SPECIAL MASTERS

Filed: March 31, 2021

* * * * * * * * * * * * * * *

KELLY RUPERT, * No. 15-841V

*

Petitioner, * Special Master Sanders

*

v. *

* Decision; Entitlement; Influenza (“Flu”)

SECRETARY OF HEALTH * Vaccine; Significant Aggravation; Kidney

AND HUMAN SERVICES, * Failure; Glomerulonephritis

*

Respondent. *

* * * * * * * * * * * * * * *

William E. Cochran, Jr., Black McLaren et al., P.C., Memphis, TN, for Petitioner.

Sarah C. Duncan, United States Department of Justice, Washington, D.C., for Respondent.

DECISION1

On August 7, 2015, Kelly Rupert (“Petitioner”) filed a petition for compensation pursuant 

to the National Vaccine Injury Compensation Program (“Program”).

2

 Pet. at 1, ECF No. 1; 42 

U.S.C. §§ 300aa-1 to 34 (2012). Petitioner alleges that the influenza (“flu”) vaccine she received 

on September 23, 2013, caused a significant aggravation of her kidney failure3 and 

glomerulonephritis. 4 Am. Pet. at 1, ECF No. 36. 

1 This Decision shall be posted on the United States Court of Federal Claims’ website, in accordance with 

the E-Government Act of 2002, 44 U.S.C. § 3501 note (2012) (Federal Management and Promotion of 

Electronic Government Services). In accordance with Vaccine Rule 18(b), a party has 14 days to identify 

and move to delete medical or other information that satisfies the criteria in § 300aa-12(d)(4)(B). Further, 

consistent with the rule requirement, a motion for redaction must include a proposed redacted decision. If, 

upon review, I agree that the identified material fits within the requirements of that provision, such 

material will be deleted from public access.

2 National Childhood Vaccine Injury Act of 1986, Pub L. No. 99-660, 100 Stat. 3755. Hereinafter, for 

ease of citation, all “§” references to the Vaccine Act will be to the pertinent subparagraph of 42 U.S.C. § 

300aa (2012).

3 Kidney failure, also called renal failure, is “the inability of a kidney to excrete metabolites at normal 

plasma levels under conditions of normal loading, or the inability to retain electrolytes under conditions 

of normal intake, so that waste products and metabolites accumulate in the blood.” Kidney Failure,

DORLAND’S MEDICAL DICTIONARY ONLINE [hereinafter “DORLAND’S”], 

https://www.dorlandsonline.com (last visited Feb. 2, 2021); Renal Failure, DORLAND’S, 

https://www.dorlandsonline.com (last visited Feb. 2, 2021).

4 Glomerulonephritis is “nephritis accompanied by inflammation of the capillary loops in the renal 

glomeruli.” Glomerulonephritis, DORLAND’S, https://www.dorlandsonline.com (last visited Feb. 2, 2021). 

Nephritis is “inflammation of the kidney[.]” Nephritis, DORLAND’S, https://www.dorlandsonline.com 

(last visited Feb. 2, 2021). Renal glomeruli are “globular tuft[s] formed by capillaries in the kidney, the 

CORRECTED
2

After carefully analyzing and weighing all the evidence and testimony presented in this 

case in accordance with the applicable legal standards, I find that Petitioner has not met her legal 

burden. Petitioner has failed to provide preponderant evidence that the flu vaccine she received on 

September 23, 2013, significantly aggravated her kidney failure or glomerulonephritis. 

Accordingly, Petitioner is not entitled to compensation. 

I. Procedural History

Petitioner filed her petition for compensation on August 7, 2015. Pet. at 1. Shortly 

thereafter, on August 10, 2015, Petitioner filed proof of her vaccination, along with ten medical 

record exhibits. Pet’r’s Exs. 1–11, ECF Nos. 6–7. The next day, Petitioner filed her firststatement 

of completion. ECF No. 8. On November 5, 2015, Respondent filed his Rule 4(c) report, 

recommending that compensation be denied. ECF No. 13. A status conference was held on 

November 23, 2015, during which Petitioner was ordered to submit an amended petition 

(clarifying the date of vaccination) by December 4, 2015, and updated medical records by January 

4, 2016. ECF No. 15. Petitioner was also ordered to file an expert report by no later than January 

25, 2016. Id.

On December 3, 2015, Petitioner filed an amended petition. ECF No. 16. Following two 

extension requests, Petitioner submitted two additional sets of medical records on March 16, 2016, 

followed by one additional set on April 6, 2016. Pet’r’s Exs. 14–16, ECF Nos. 21, 26. Petitioner 

filed her second statement of completion on April 6, 2016. ECF No. 27.

Petitioner submitted an expert report from Eric Gershwin, M.D., accompanied by

supporting medical literature, on April 15, 2016. Pet’r’sExs. 19–46, ECF Nos. 28–31. On the same 

date, Petitioner filed an opinion letter from Wesam Ballouk, M.D. ECF No. 28. On July 21, 2016, 

Respondent filed two responsive expert reports, one from Arnold Levinson, M.D., and one from 

Derek Fine, M.D., along with fourteen pieces of supporting medical literature. Resp’t’s Exs. A–D, 

ECF Nos. 33-1, 34-2–34-3, 34-8; Resp’t’s Ex. A, Tabs 1–10, ECF Nos. 33-2–34-1; Resp’t’s Ex. 

C, Tabs 1–4, ECF Nos. 34-4–34-7.

The parties convened for a status conference on July 27, 2016, at which time Petitionerwas 

ordered to file a second amended petition (to limit her claim to significant aggravation) and 

updated medical records. ECF No. 35. Petitioner filed a second amended petition and the requested

medical records on August 30, 2016. ECF Nos. 36–37.

On January 3, 2017, Petitioner filed a supplemental expert report from Dr. Gershwin along 

with a supplemental opinion letter from Dr. Ballouk. Pet’r’sExs. 49–50, ECF No. 40-1–40-2. The 

case was reassigned to me on January 9, 2017. ECF No. 41. On February 17, 2017, Respondent 

filed a responsive supplemental expert report from Dr. Fine. Resp’t’s Ex. E, ECF No. 43-1. 

On July 5, 2017, I issued an order directing the parties to file a status report with proposed

dates for an entitlement hearing. Scheduling Order, docketed July 5, 2017. The matter was 

subsequently set for a hearing on December 5–6, 2018. ECF Nos. 51–52. The hearing date was 

site of the filtration barrier between the blood and the kidney[.]” Renal Glomerulus, DORLAND’S, 

https://www.dorlandsonline.com (last visited Feb. 2, 2021).
3

subsequently rescheduled to October 29–30, 2019, due to the funeral of former President of the 

United States George H.W. Bush. ECF No. 71. The entitlement hearing was held as scheduled on 

these dates. See Min. Entry, docketed Oct. 31, 2019.

This matter is now ripe for consideration.

II. Factual Background

A. Medical Records

Petitioner was born on March 17, 1968. E.g., Pet. at 1. Petitioner’s pre-vaccination medical 

history is notable for hypertension,5 edema,6 obesity, smoking,

7 pain, and anxiety. See generally 

Pet’r’s Ex. 1. Petitioner’s first record from Raymond Nino, M.D., a primary care physician

(“PCP”), is from August 10, 2010. See id. at 36. Petitioner’s blood pressure readings were 

relatively stable and within or near normal range8 until July 12, 2011, when her provider reported 

a spike at 138/90.9Id. at 28; see also id. at 29–36. Also on July 12, 2011, Petitioner’s provider 

noted that she had edema. Id. at 28. Although Petitioner’s blood pressure was sometimes normal 

after this occasion, it continued to spike at times between 2011 and 2013. See id. at 1–27.It reached 

a high of 176/124 on August 20, 2013. Id. at 4. On that date, Petitioner also complained of leg and 

back pain, which she rated as a two out of ten on a pain scale. Id. Dr. Nino assessed Petitioner with 

5 Hypertension is “high arterial blood pressure; various criteria for its threshold have been suggested, 

ranging from 140 mm Hg systolic and 90 mm Hg diastolic to as high as 200 mm Hg systolic and 110 mm 

Hg diastolic. Hypertension may have no known cause . . . or be associated with other primary diseases.” 

Hypertension, DORLAND’S, https://www.dorlandsonline.com (last visited Feb. 7, 2021).

6 Edema, also called dropsy or hydrops, is “the presence of abnormally large amounts of fluid in the 

intercellular tissue spaces of the body, usually referring to subcutaneous tissues.” Edema, DORLAND’S, 

https://www.dorlandsonline.com (last visited Feb. 7, 2021).

7 Petitioner testified that she quit smoking in the fall of 2013. Tr. 33:16–18. 

8 The Centers for Disease Control and Prevention (“CDC”) states that “[a] normal blood pressure is less 

than 120/80 mmHg.” High Blood Pressure Symptoms and Causes, CENTERS FOR DISEASE CONTROL AND 

PREVENTION, https://www.cdc.gov/bloodpressure/about.htm (last visited Feb. 19, 2021). 

9 As indicated in Dorland’s, supra note 5, there is not a universal cutoff used to identify hypertension. See 

High Blood Pressure Symptoms and Causes, CENTERS FOR DISEASE CONTROL AND PREVENTION, 

https://www.cdc.gov/bloodpressure/about.htm (last visited Feb. 19, 2021). The CDC refers to two 

different guidelines, one from 2003 and another from 2017. Id. The 2003 guideline (“The Seventh Report 

of the Joint National Committee on Prevention, Detection, Evaluation, and Treatment of High Blood 

Pressure”) indicates that high blood pressure, or hypertension, is 140 mm Hg or higher systolic and 90 

mm Hg or higher diastolic. Id. Said guideline also indicates that 120–139 mm Hg systolic and 80–89 mm 

Hg diastolic is “elevated” and qualifies as prehypertension. Id. The 2017 guideline (“The American 

College of Cardiology/American Heart Association Guideline for Prevention, Detection, Evaluation, and 

Management of High Blood Pressure in Adults”) identifies hypertension as 130 mm Hg or higher systolic 

and 80 mm Hg or higher diastolic. Id. It indicates that 120–129 mm Hg systolic with less than 80 mm Hg 

diastolic is elevated. Id. 
4

“[osteoarthritis10 (“OA”) of her lumbar] spine11” and gave her a 120-count refill for her 

Roxicodone12 prescription. Id. The records from Dr. Nino indicate that Petitioner regularly took 

Roxicodone and sometimes took Xanax.13 See generally Pet’r’s Ex. 1. Petitioner’s provider also 

noted that she had edema on May 24, 2012, June 26, 2012, and May 20, 2013. Id. at 6, 18–19. 

Petitioner received the flu vaccination at issue at a Rite Aid on September 23, 2013. Pet’r’s 

Ex. 2 at 1. On October 1, 2013, Petitioner attended a follow-up appointment with Dr. Nino. Id. at 

3. Petitioner again complained of back and left leg pain, but she rated said pain, when she took her 

Roxicodone prescription as directed, as a zero on the pain scale. Id. Petitioner also complained of 

anxiety. Id. She further complained of one day of mild vaginal bleeding, which she reported had 

occurred the previous month. Id. Petitioner explained that her “last menstrual period was [in] 

September 2012.” Id. She was assessed with “OA L[-]Spine,” anxiety, and vaginal bleeding. Id.

She was given another 120-count Roxicodone prescription refill, a 90-count Xanax prescription

refill and instructed to follow up with a gynecologist. Id.

Petitioner attended another follow-up appointment with Dr. Nino on November 7, 2013. 

Id. at 2. Petitioner again complained of left leg and back pain. Id. Petitioner voiced no other 

complaints at this visit. Id. Dr. Nino assessed Petitioner with OA of her lumbar spine and gave 

Petitioner another 120-count refill of her Roxicodone prescription. Id.

On November 21, 2013, Petitioner presented to the emergency room at Monongahela 

Valley Hospital (“MVH”) “with complaints of having abdominal pain, nausea, vomiting and 

diarrhea for the last two weeks.” Pet’r’s Ex. 3(b) at 289. Doctors noted that Petitioner’s abdominal 

pain was “in the periumbilical14 region[,]” and that Petitioner rated the pain as a five out of ten on 

the pain scale. Id. Petitioner stated that “once she vomits and passes diarrhea then her abdominal 

pain [is] relieve[d] to a certain extent.” Id. Petitioner further explained that “[s]he feels nauseated 

10 Osteoarthritis is “a noninflammatory degenerative joint disease seen mainly in older persons, 

characterized by degeneration of the articular cartilage, hypertrophy of bone at the margins, and changes 

in the synovial membrane. It is accompanied by pain . . . and stiffness . . . .” Osteoarthritis, DORLAND’S, 

https://www.dorlandsonline.com (last visited Feb. 2, 2021).

11 The lumbar spine is “the part of the spine comprising the lumbar vertebrae[,]” which are “the five 

vertebrae[,]” labeled L1 through L5 “between the thoracic vertebrae and the sacrum.” Lumbar Spine, 

DORLAND’S, https://www.dorlandsonline.com (last visited Feb. 2, 2021); Lumbar Vertebrae, 

DORLAND’S, https://www.dorlandsonline.com (last visited Feb. 2, 2021); Vertebrae Lumbales, 

DORLAND’S, https://www.dorlandsonline.com (last visited Feb. 2, 2021).

12 Roxicodone is a trademark for oxycodone hydrochloride, which is “the hydrochloride salt of 

oxycodone, used as an analgesic[.]” Oxycodone is an “opioid agonist analgesic . . . .” Roxicodone, 

DORLAND’S, https://www.dorlandsonline.com (last visited Feb. 2, 2021); Oxycodone Hydrochloride, 

DORLAND’S, https://www.dorlandsonline.com (last visited Feb. 2, 2021); Oxycodone, DORLAND’S, 

https://www.dorlandsonline.com (last visited Feb. 2, 2021).

13 Xanax is a trademark for alprazolam, which is “a short-acting benzodiazepine used as an antianxiety 

agent in the treatment of anxiety disorders and panic disorders and for short-term relief of anxiety 

symptoms . . . .” Xanax, DORLAND’S, https://www.dorlandsonline.com (last visited Feb. 2, 2021); 

Alprazolam, DORLAND’S, https://www.dorlandsonline.com (last visited Feb. 2, 2021).

14 Periumbilical means “near or around the umbilicus[,]” which is the navel. Periumbilical, DORLAND’S, 

https://www.dorlandsonline.com(last visited Feb. 2, 2021); Umbilicus, DORLAND’S, 

https://www.dorlandsonline.com (last visited Feb. 2, 2021).
5

and . . . vomits [one]-[two] times a day[,]” and that she has “diarrhea [three]-[four] times in a day.” 

Id. CT scans of Petitioner’s abdomen and pelvis conducted while she was in the emergency room 

“revealed no evidence of calculus15 or hydronephrosis,16” and Petitioner’s “appendix was . . . 

normal.” Id. In addition, doctors wrote that “[t]here was no evidence of inflammatory bowel 

disease17” and that Petitioner’s uterus and adnexa were also normal. Id. Lastly, doctors noted that 

Petitioner’s “BUN18 was . . . [thirty-three] with [her] creatinine19 [at] 2.8.” Id. Both results were 

classified as high. See id. at 283. Additionally, Petitioner’s urinalysis revealed high protein levels 

at greater than 300 mg/dl as well as the presence of blood and red blood cells. Id. Doctors assessed 

Petitioner with, among other things, abdominal pain of a “not very clear” etiology, diarrhea with 

a “not very obvious” etiology, dehydration, and chronic back pain. Id. at 292. They determined

that Petitioner would “continue with her pain medications.” Id. In addition, doctors assessed 

Petitioner with “[r]enal insufficiency [that] appears to be acute renal insufficiency20 because of 

dehydration.” Id. They noted that they would continue to monitor Petitioner’s BUN and creatinine 

and proceeded to schedule a nephrology consultation for the next day. Id. Petitioner was admitted 

for further observation. Id. However, the next day, Petitioner checked herself out of the hospital 

against medical advice. Id. at 288.

Petitioner presented to Dr. Nino for a follow-up appointment on December 10, 2013. 

Pet’r’s Ex. 1 at 1. Petitioner complained of back and left leg pain but did not voice any additional 

complaints. Id. Dr. Nino did not make any notations or statements regarding Petitioner’s recent 

hospitalization. See id. Dr. Nino’s only assessment was OA of Petitioner’s lumbar spine. Id. He 

provided Petitioner an additional 120-count refill of her Roxicodone prescription. Id.

On January 22, 2014, Petitioner presented to a new PCP, Joanna Swauger, D.O., to 

establish care. Pet’r’s Ex. 12 at 30. Petitioner stated that “she went to the ER this fall, for abdominal 

pain. [She w]as told that she was severely dehydrated and given [three] liters of NSS.” Id.

15 Calculus, or stone, is “an abnormal concretion in the body, usually composed of mineral salts.” 

Calculus, DORLAND’S, https://www.dorlandsonline.com (last visited Feb. 2, 2021).

16 Hydronephrosis is “distention of the pelvis and calices of the kidney with urine, as a result of 

obstruction of the ureter[,]” which is “the fibromuscular tube that conveys the urine from the kidney to the 

bladder.” Hydronephrosis, DORLAND’S, https://www.dorlandsonline.com (last visited Feb. 2, 2021); 

Ureter, DORLAND’S, https://www.dorlandsonline.com (last visited Feb. 2, 2021).

17 Inflammatory bowel disease is “a general term for those inflammatory diseases of the intestines that 

have an unknown etiology . . . .” Inflammatory Bowel Disease, DORLAND’S, 

https://www.dorlandsonline.com (last visited Feb. 2, 2021).

18 BUN is “blood urea nitrogen[.]” BUN, DORLAND’S, https://www.dorlandsonline.com (last visited Feb. 

2, 2021).

19 Creatinine is “the cyclic anhydride of creatine, produced as the final product of decomposition of 

phosphocreatine[]” and “is excreted in the urine.” Creatinine, DORLAND’S, 

https://www.dorlandsonline.com (last visited Feb. 3, 2021).

Creatine is “an amino acid formed by methylation of guanidinoacetic acid, found in vertebrate tissues, 

particularly in muscle.” Creatine, DORLAND’S, https://www.dorlandsonline.com (last visited Feb. 3, 

2021).

20 Renal insufficiency is “a state of disordered function of the kidneys verifiable by quantitative tests[]” 

that “may progress to renal failure.” Renal Insufficiency, DORLAND’S, https://www.dorlandsonline.com

(last visited Feb. 2, 2021). “Acute” refers to “a short and relatively severe course.” Acute, DORLAND’S, 

https://www.dorlandsonline.com (last visited Feb. 2, 2021).
6

Petitioner further stated that her nausea and vomiting “resolved.” Id. Petitioner noted that “she has 

been having issues with her back,” although she explained that her recent weight loss had “really 

helped to decrease her back pain.” Id. Petitioner’s blood pressure was elevated at 160/110. Id. at 

31. At this visit, Petitioner underwent a urinalysis, which revealed high levels of potassium, BUN, 

and creatinine. Pet’r’s Ex. 3(a) at 5. Dr. Swauger wrote that Petitioner had an “[o]verall normal 

exam, aside from [blood pressure] and [urinalysis]. Will obtain old records and [follow up] 

accordingly.” Pet’r’s Ex. 12 at 31. Regarding Petitioner’s back pain, Dr. Swauger wrote that she 

“encourage[d Petitioner to] use her Oxycodone sparingly. Advised her that the [fifteen milligram] 

dose is rather high, and that if she will require frequent use, she may need to be referred to [a] pain 

clinic.” Id. at 32. Dr. Swauger also wrote that she would “send [Petitioner’s urinalysis] for 

eval[uation] at [the] lab . . . [to] rule out [infection]. If negative, will need to obtain [ultrasounds] 

of [her] kidneys for eval[uation] and possibly [obtain a] consultation by [a] nephrologist.” Id. Dr. 

Swauger directed Petitioner to follow up in four weeks. Id.

Petitioner underwent ultrasounds of her kidneys on January 29, 2014. Pet’r’s Ex. 3(a) at 

16. The ultrasounds revealed “mild prominence of the renal pyramids 21 bilaterally. This may 

reflect papillary necrosis.22” Id. Petitioner also underwent a thyroid ultrasound on this date. Id. at 

17. The impression of this test was a “[m]ultinodular thyroid.” Id. Also, on this date, Dr. Swauger 

received the lab results of Petitioner’s urinalysis, which showed that “the total protein was 11,365.” 

Pet’r’s Ex. 12 at 27. In response, Dr. Swauger wrote the following:

I have not seen her old records, so not sure how long this has been going on with 

her kidneys. Her [blood work] from today shows that her creatinine is about the 

same as last week – abnormal at 3.5 (last week was 3.6) . . . . Please tell [Petitioner] 

that her kidneys are leaking too much protein, and that this needs to be addressed 

ASAP. . . . I see that she had [ultrasounds] of the kidneys. It looks like they are 

normal in size and shape, but the center of them looks like they may have something 

called “papillary necrosis.” This can have various causes, but [it] is commonly 

caused by overuse of pain med[ications]. So [she should] try to avoid them at all 

cost for now and go see the kidney [doctors] for [an] eval[uation].

Id. Dr. Swauger also noted that Petitioner’s thyroid ultrasound “showed . . . a couple nodules” that 

were concerning, and Dr. Swauger thought they “need[ed] to be biopsied.” Id. Dr. Swauger’s nurse 

wrote in the same note that she had spoken with Petitioner, and Petitioner had stated that “she has 

not taken any form of pain med[ication] since she received the news about her kidneys.” Id.

Petitioner also indicated that “she want[ed] to get to the bottom of [her] kidney problems before 

she does anything with [her] thyroid.” Id. 

21 Renal pyramids are “the conical masses that make up the substance of the renal medulla[,]” which is 

“the inner part of the substance of the kidney . . . .” Pyramides Renales, DORLAND’S, 

https://www.dorlandsonline.com (last visited Feb. 2, 2021); Renal Medulla, DORLAND’S, 

https://www.dorlandsonline.com (last visited Feb. 2, 2021).

22 Papillary “pertain[s] to or resembl[es] a papilla,” which is “a small nipple-shaped projection, elevation, 

or structure.” Papillary, DORLAND’S, https://www.dorlandsonline.com (last visited Feb. 3, 2021).

Necrosis is “the sum of morphologic changes indicative of cell death and caused by the progressive 

degradation action of enzymes[.]” Necrosis, DORLAND’S, https://www.dorlandsonline.com (last visited 

Feb. 3, 2021).
7

On January 30, 2014, Petitioner presented to Ronald Lutes, D.O., a nephrologist, for a 

consultation. Pet’r’s Ex. 9 at 1. Dr. Lutes wrote that “[s]everal months ago[, Petitioner] had severe 

[vomiting/diarrhea,] which has since resolved. She has been feeling well.” Id. at 3. Dr. Lutes 

reviewed Petitioner’s prior lab work and conducted a physical examination, which was 

unremarkable. Id. at 3–4. Dr. Lutes assessed Petitioner with proteinuria,

23 chronic kidney disease 

(“CKD”)24- stage IV, and hematuria.25 Id. at 1. Dr. Lutes wrote that Petitioner had “[p]rogressive 

renal dysfunction with nephrotic range proteinuria and hematuria.” Id. He also wrote that he 

“strongly suspect[ed] a glomerulonephritis[,]” and he believed that “[t]he most likely diagnosis at 

this time would be one of proliferative glomerulonephritis26 and a concern towards a vasculitic 

process[,] i.e. lupus or a[n] Anca[-]associated process.27” Id. Dr. Lutes also noted that Petitioner 

may need to undergo a renal biopsy. Id.

Petitioner underwent a left renal biopsy on February 19, 2014. Pet’r’s Ex. 3(a) at 62, 70–

71, 102–03. Prior to the biopsy, Petitioner told doctors “that she had a flu shot sometime in October 

and . . . that she had not been feeling well since that time.” Id. at 70. The biopsy revealed “a 

fibrillary glomerulonephritis [(“FGN”)]28[] that is associated with extensive chronic changes 

23 Proteinuria, also called albuminuria, is “excessive serum proteins in the urine, such as in renal disease, 

after strenuous exercise, and with dehydration. Proteinuria, DORLAND’S, 

https://www.dorlandsonline.com (last visited Feb. 2, 2021).

24 Chronic kidney disease, or chronic renal failure, is “gradual loss of kidney function, with progressively 

more severe renal insufficiency . . . .” Chronic Kidney Disease, DORLAND’S, 

https://www.dorlandsonline.com (last visited Feb. 4, 2021).

25 Hematuria, also called erythrocyturia, refers to “blood (erythrocytes) in the urine[.]” Hematuria, 

DORLAND’S, https://www.dorlandsonline.com (last visited Feb. 2, 2021). Erythrocytes are “one of the 

elements found in peripheral blood.” Erythrocyte, DORLAND’S, https://www.dorlandsonline.com (last 

visited Feb. 4, 2021).

26 Proliferative Glomerulonephritis refers to “any of various types accompanied by proliferation of 

endothelial or mesangial cells in the glomeruli . . . .” Proliferative Glomerulonephritis, DORLAND’S, 

https://www.dorlandsonline.com (last visited Feb. 2, 2021). Endothelial refers to the endothelium, “the 

layer of epithelial cells that lines the interior structures such as the cavities of the heart, the lumina of 

blood and lymph vessels, and the serous cavities of the body[.]” Endothelium, DORLAND’S, 

https://www.dorlandsonline.com (last visited Feb. 3, 2021).

Mesangial refers to the mesangium, “the thin membrane that helps support the capillary loops in the renal 

glomerulus.” Mesangium, DORLAND’S, https://www.dorlandsonline.com (last visited Feb. 3, 2021).

27 ANCA-associated vasculitis is “a subgroup of small vessel vasculitis in which there are circulating 

antineutrophil cytoplasmic autoantibodies (ANCA) . . . .” ANCA-Associated Vasculitis, DORLAND’S, 

https://www.dorlandsonline.com (last visited Feb. 2, 2021). Vasculitis is “inflammation of a blood or 

lymph vessel[.]” Vasculitis, DORLAND’S, https://www.dorlandsonline.com (last visited Feb. 2, 2021).

ANCA, also called antineutrophil cytoplasmic autoantibody, is “an autoantibody to cytoplasmic 

constituents of monocytes and neutrophils, found in increased amounts in some types of vasculitis[]” 

which has “several different subtypes, each characterized serologically by reactivity against particular 

cellular antigens[.]” ANCA, DORLAND’S, https://www.dorlandsonline.com (last visited Feb. 2, 2021); 

Antineutrophil Cytoplasmic Autoantibody, DORLAND’S, https://www.dorlandsonline.com (last visited 

Feb. 3, 2021).

28 Fibrillary glomerulonephritis is “a rare form of glomerulonephritis characterized by infiltration of the 

glomeruli with fibrils slightly larger than amyloid fibrils that do not stain with Congo red.” Fibrillary 

Glomerulonephritis, DORLAND’S, https://www.dorlandsonline.com (last visited Feb. 2, 2021). Fibrils are 
8

involving all components of the parenchyma29 including focal global glomerulosclerosis,30

extensive tubular atrophy and interstitial fibrosis,31 and moderately severe vascular sclerosis.32” 

Id. at 95. It also showed “extensive interstitial inflammation . . . .” Id. Petitioner’s biopsy revealed 

that eighteen out of twenty-three of her present glomeruli were globally sclerosed. Id. Additionally:

[T]hree glomeruli show segmental sclerosis, with segmental adhesion of the 

glomerular tufts to the Bowman’s capsule.33 The glomeruli do not show any 

“minute filament[s], such as a component of fiber.” Fibril, DORLAND’S, https://www.dorlandsonline.com 

(last visited Feb. 3, 2021). Amyloid, deposits of which are primarily composed of fibrils, is “a waxy 

eosinophilic substance deposited in amyloidosis.” Amyloid, DORLAND’S, https://www.dorlandsonline.com 

(last visited Feb. 3, 2021). Amyloidosis refers to “a group of conditions of diverse etiologies characterized 

by the accumulation of insoluble amyloid in various organs and tissues of the body, which compromises 

vital function.” Amyloidosis, DORLAND’S, https://www.dorlandsonline.com (last visited Feb. 2, 2021).

Congo red refers to a powder used “as a diagnostic aid in amyloidosis.”

Congo Red, DORLAND’S, https://www.dorlandsonline.com (last visited Feb. 2, 2021).

29 Parenchyma refers to “the essential or functional elements of an organ, as distinguished from its 

framework (stroma).” Parenchyma, DORLAND’S, https://www.dorlandsonline.com (last visited Feb. 2, 

2021).

30 Glomerulosclerosis is “fibrosis and scarring with senescence of the renal glomeruli.” 

Glomerulosclerosis, DORLAND’S, https://www.dorlandsonline.com (last visited Feb. 2, 2021). Fibrosis 

refers to “the formation of fibrous tissue, as in repair or replacement of parenchymatous elements.” 

Fibrosis, DORLAND’S, https://www.dorlandsonline.com (last visited Feb. 2, 2021).

31 Interstitial fibrosis refers to idiopathic pulmonary fibrosis, a “chronic inflammation and progressive 

fibrosis of the pulmonary alveolar walls, with steadily progressive dyspnea, resulting finally in death from 

oxygen lack or right heart failure.” Interstitial Fibrosis, DORLAND’S, https://www.dorlandsonline.com 

(last visited Feb. 2, 2021). Pulmonary “pertain[s] to the lungs.” Pulmonary, DORLAND’S, 

https://www.dorlandsonline.com (last visited Feb. 3, 2021). Dyspnea is “breathlessness or shortness of 

breath[.]” Dyspnea, DORLAND’S, https://www.dorlandsonline.com (last visited Feb. 3, 2021).

32 Vascular sclerosis refers to arteriosclerosis, which is “any of a group of diseases characterized by 

thickening and loss of elasticity of arterial walls[.]” Arteriosclerosis, DORLAND’S, 

https://www.dorlandsonline.com (last visited Feb. 2, 2021).

33 The glomerular capsule, also known as the Bowman, malpighian, or müllerian capsule, is “the doublewalled globular dilatation that forms the beginning of a renal tubule and surrounds the glomerulus; the 

inner wall is called the visceral layer and the outer wall is called the parietal layer.” Capsula Glomeruli, 

DORLAND’S, https://www.dorlandsonline.com (last visited Feb. 3, 2021).
9

evidence of crescent34 formation, fibroid necrosis,35 thrombosis,36 or endocapillary 

proliferation. The glomerular basement membranes37 appear thickened . . . . The 

interstitial infiltrates contain mostly mononuclear cells. In one area, there is 

formation of a small granuloma38 with giant cells. There is also extensive tubular 

atrophy . . . .

Id. at 95–96.

On February 28, 2014, Petitioner presented to another nephrologist, Sudha M. Nayar, 

M.D.,39 for a follow-up. Pet’r’s Ex. 9 at 6. Dr. Nayar reviewed Petitioner’s biopsy results with her, 

noting that it showed “[f]ibrillary [g]lomerulonephritis, that is associated with extensive chronic 

changes involving all components of the parenchyma . . . .” Id. Dr. Nayar further noted that the 

“light microscopic features do[] not show any evidence of [membranoproliferative

glomerulonephritis (“MPGN”)40], crescents or proliferative GN.” Id. However, Dr. Nayar wrote

that the biopsy did “show[] extensive tubular atrophy and fibrosis[,] but some areas show 

interstitial inflammation and infiltration with mononuclear cells.” Id. She then discussed treatment 

options, including an “immunosuppressive regimen,” but noted that she was “not sure if 

immunosuppressive regimen would help delay the progression of the eventual [end -stage renal 

34 An epithelial crescent is “a more or less crescentic mass of cells found between the tuft of a glomerulus 

and the inside of Bowman capsule in rapidly progressive glomerulonephritis.” Epithelial Crescent, 

DORLAND’S, https://www.dorlandsonline.com (last visited Feb. 4, 2021). Rapidly progressive 

glomerulonephritis is “acute glomerulonephritis marked by a rapid progression to end-stage renal disease 

. . . .” Rapidly Progressive Glomerulonephritis, DORLAND’S, https://www.dorlandsonline.com (last 

visited Feb. 4, 2021).

35 Fibrinoid necrosis, also known as necrotizing arteriolitis, is “deposition of fibrin and other plasma 

proteins in the walls of afferent renal arterioles in malignant hypertension, often accompanied by an 

inflammatory infiltrate within the walls and thrombosis of the vessel lumen.” Fibrinoid Necrosis, 

DORLAND’S, https://www.dorlandsonline.com (last visited Feb. 3, 2021). Fibrin is “the insoluble protein 

from fibrinogen by the proteolytic action of thrombin during normal clotting of blood; it forms the 

essential portion of the blood clot.” Fibrin, DORLAND’S, https://www.dorlandsonline.com (last visited 

Feb. 3, 2021). An arteriole, or arteriola, is “a minute arterial branch, especially one just proximal to a 

capillary.” Arteriola, DORLAND’S, https://www.dorlandsonline.com (last visited Feb. 3, 2021).

36 Thrombosis is “the formation, development, or presence of a thrombus[,]” which is “a stationary blood 

clot along the wall of a blood vessel” that “frequently caus[es] vascular obstruction.” Thrombosis, 

DORLAND’S, https://www.dorlandsonline.com (last visited Feb. 3, 2021); 

Thrombus, DORLAND’S, https://www.dorlandsonline.com (last visited Feb. 3, 2021).

37 A basement membrane is “a thin sheet of amorphous extracellular material upon which the basal 

surfaces of epithelial cells rest[]” and “is interposed between the cellular elements and the underlying 

connective tissue.” Basement Membrane, DORLAND’S, https://www.dorlandsonline.com (last visited Feb. 

3, 2021). 

38 Granuloma is “an imprecise term applied to either a small, nodular, delimited aggregation of 

mononuclear inflammatory cells or a similar collection of epithelioid cells[.] . . . Granuloma formation 

represents a chronic inflammatory response that can be initiated by infectious or noninfectious agents.” 

Granuloma, DORLAND’S, https://www.dorlandsonline.com (last visited Mar. 30, 2021).

39 Dr. Nayar worked in the same practice as Dr. Lutes. See Pet’r’s Ex. 9 at 6. 

40 Membranoproliferative glomerulonephritis is “a chronic glomerulonephritis characterized by mesangial 

cell proliferation and irregular thickening of the glomerular capillary wall.” Membranoproliferative 

Glomerulonephritis, DORLAND’S, https://www.dorlandsonline.com (last visited Feb. 2, 2021).
10

disease (“ESRD”)41].” Id. Dr. Nayar recommended “weekly bloodwork to closely monitor

[Petitioner’s] renal function.” Id. at 7. Dr. Nayar further discussed with Petitioner the possibility 

of “renal replacement therapy including hemodialysis42 and peritoneal dialysis[.]

43” Id. Petitioner 

expressed a desire to obtain a second opinion, and Dr. Nayar agreed that she should. Id. 

Petitioner’s medical records contain an undated note recounting a phone message Dr. 

Nayar left for Dr. Swauger. Pet’r’s Ex. 12 at 26. Dr. Nayar stated that she “got [the] results of 

[Petitioner’s kidney biopsy], which showed a lot of fibrosis.” Id. Therefore, Dr. Nayar thought 

“that this may have been ongoing longer.” Id. Dr. Nayar noted that the biopsy “revealed a type 

of proliferative GN, with fibrosis [that] can be assoc[iated] with malignancy or myeloproliferative 

disorder.44” Id. Dr. Nayar further noted that Petitioner’s creatinine “seems to be worsening, [and 

was] now up to 3.9.” Id. Dr. Nayar explained that Petitioner “may be a candidate for 

immunosuppressive/steroids for [treatment], but [Dr. Nayar was] not sure it will be effective . . .

.” Id. After reviewing Petitioner’s other results, Dr. Nayar concluded by recommending that 

Petitioner stop taking her Oxycodone immediately. Id. 

On March 4, 2014, Petitioner presented to Dr. Swauger for a follow-up.Id. at 23. Petitioner 

stated that, despite extensive bloodwork and a kidney biopsy, her nephrologists “are not certain 

what the source of her kidney failure is from.” Id. Petitioner told Dr. Swauger that “overall she 

feels well.” Id. In addition, Petitioner told Dr. Swauger that “[s]he was told to have a cancer 

[workup], as underlying malignancy may be the source of [her] . . . problem[s].” Id. Dr. Swauger 

recommended that Petitioner undergo a chest x-ray and a biopsy of her thyroid nodule. Id. at 23–

24. Petitioner underwent a chest x-ray on March 10, 2014, which was unremarkable. Pet’r’s Ex. 

3(a) at 158. Petitioner subsequently underwent a thyroid biopsy on March 21, 2014, which was 

“negative for malignant cells.” Pet’r’s Ex. 6(b) at 305, 311–13.

Petitioner had another follow-up appointment with Dr. Nayar on March 31, 2014. Pet’r’s 

Ex. 9 at 12. Petitioner reported “feeling well” and having “good” urine output. Id. She did not 

report experiencing any nausea, vomiting, or diarrhea, and did not have any edema on examination. 

Id. Petitioner told Dr. Nayar that she had an appointment scheduled with transplant services the 

following month. Id. Petitioner also stated that she “talked with the [peritoneal dialysis (“PD”)] 

nurse, and if needed[,] she would rather do PD.” Id. 

41 End-stage renal disease is “chronic renal failure that is irreversible.” End-Stage Renal Disease, 

DORLAND’S, https://www.dorlandsonline.com (last visited Feb. 4, 2021).

42 Hemodialysis is “the removal of certain elements from the blood by virtue of the difference in the rates 

of their diffusion through a semipermeable membrane.” Hemodialysis, DORLAND’S, 

https://www.dorlandsonline.com (last visited Feb. 2, 2021).

43 Peritoneal dialysis is “hemodialysis through the peritoneum[,]” which is “the serious membrane lining 

the walls of the abdominopelvic cavity . . . and investing the viscera . . . .” Peritoneal Dialysis, 

DORLAND’S, https://www.dorlandsonline.com/dorland/definition?id=33488&searchterm=nephritis (last 

visited Feb. 2, 2021); Peritoneum, DORLAND’S, https://www.dorlandsonline.com (last visited Feb. 3, 

2021).

44 Myeloproliferative disorders are “a group of usually neoplastic diseases, which may be related 

histogenetically by a common multipotential stem cell . . . .” Myeloproliferative Disorders, DORLAND’S, 

https://www.dorlandsonline.com (last visited Feb. 3, 2021).
11

On May 31, 2014, Petitioner presented to Dr. Nayar for a follow-up. Id. at 16. Dr. Nayar 

wrote that Petitioner “has had worsening of her [r]enal functions, [with her] BUN [at ninety-five], 

creatinine [at] 5.4[, potassium] . . . at 5.4[, and] PO4 . . . [at] 6.6.” Id. Dr. Nayar recommended that 

Petitioner “get the PD catheter45 placed.” Id. 

Petitioner presented to Dr. Swauger on June 4, 2014, for a follow-up. Pet’r’s Ex. 12 at 19. 

Petitioner did not complain of any “symptoms aside from continuous[,] unexplained weight loss.” 

Id. Dr. Swauger noted that Petitioner’s “[k]idney function has continue[d] to progressively decline, 

although she denies swelling, [shortness of breath], [and] fatigue.” Id. Petitioner reported that she 

was scheduled to have a PD catheter placed later that month. Id. Dr. Nayar “[r]ecommended that 

[Petitioner] be vaccinated for [Hepatitis A and B], [measles, mumps, and rubella,] . . . Varicella[,] 

and obtain a [tetanus-diphtheria-acellar-pertussis]. . . particularly if she is anticipating a transplant, 

which will be followed by immune suppressive medications.” Id. at 20. Petitioner agreed to 

consider getting these vaccinations but declined them on that date. Id. 

On June 9, 2014, Petitioner presented to Dr. Nayar for a follow-up. Pet’r’s Ex. 9 at 20. Dr. 

Nayar noted that Petitioner’s “[r]enal function continues to worsen . . . .” Id. Petitioner’s creatinine 

was 6.6. Id. Petitioner did not report any complaints and “denie[d] any uremic 46 symptoms.” Id.

Dr. Nayar wrote that Petitioner was “scheduled to . . . undergo PD cath[eter] placement on the 18th

[of that month].” Id. Dr. Nayar continued, “[i]f [Petitioner’s] labs worsen, then we will have [the 

surgeon] place an exposed catheter and begin [dialysis] in [two] weeks. Otherwise we will keep it 

buried until RRT is needed.” Id. Dr. Nayar directed Petitioner to follow up again in three weeks. 

Id.

Petitioner had a PD catheter placed on June 18, 2014, and began PD the same day. Pet’r’s 

Ex. 4 at 2–3. Both her pre-operative and post-operative diagnoses were listed as “[e]nd-stage renal 

failure.” Id. at 2. On July 12, 2014, Petitioner presented to the emergency room “to get [her PD] 

catheter checked.” Id. Petitioner explained that she “usually do[es her PD with] gravity[,]” but she 

had “used a circulator for the first time [that] morning and . . . [thought] it was too much . . . .” Id.

at 25. Petitioner further explained that doctors had “increased [her dialysis] fluids to 1500 

[milliliters six] days ago.” Id. Petitioner was examined and released the same day. See id. at 25–

41.

On August 22, 2014, Petitioner underwent a chest x-ray. Pet’r’s Ex. 3 at 276. The results 

showed “mild emphysema47 . . .” and “a [three millimeter,] possibly calcified pulmonary nodule 

laterally within the left upper lobe, likely benign but follow[-]up recommended.” Id. at 277. They 

45 A catheter is “a tubular, flexible, surgical instrument that is inserted into a cavity of the body to 

withdraw or introduce fluid.” Catheter, DORLAND’S, https://www.dorlandsonline.com (last visited Feb. 4, 

2021).

46 Uremia refers to “the entire constellation of signs and symptoms of chronic renal failures, including

nausea, vomiting, anorexia, a metallic taste in the mouth, a characteristic odor of the breath, pruritus, urea 

frost on the skin, neuromuscular disorders, pain and twitching in the muscles, hypertension, edema, 

mental confusion, and acid-base and electrolyte imbalances.” Uremia, DORLAND’S, 

https://www.dorlandsonline.com(last visited Feb. 3, 2021).

47 Emphysema is “a pathologic accumulation of air in tissues or organs.” Emphysema, DORLAND’S, 

https://www.dorlandsonline.com (last visited Feb. 2, 2021).
12

also showed “a 1.9 [by] 1.6 [centimeter] right thyroid nodule for which ultrasound correlation and 

likely biopsy [are] recommended.” Id. 

Petitioner was transported to the emergency room after suffering a seizure on August 26, 

2014. Pet’r’s Ex. 5 at 78. Petitioner’s sister stated that Petitioner “ha[d] not been complaining of 

anything recently. She has not recently been sick, though the dialysis does make [her] vomit daily.” 

Id. Petitioner’s husband explained that Petitioner “was somewhat ill throughout the day with 

anorexia[,] which progressed to vomiting and some [altered mental status] . . . .” Id. at 76. He 

stated that Petitioner “then had [a] seizure [and] fell [and] hit her head.” Id. While being treated 

by emergency medical services (“EMS”), Petitioner “was very combative and had a second seizure 

. . . .” Id. After her second seizure, Petitioner “was again very combative and was intubated for 

airway protection [and given rapid sequence intubation (“RSI”)] drugs . . . .” Id. On arrival at the 

emergency room, Petitioner was “intubated, sedated on Propofol,48 and paralyzed.” Id. Petitioner’s 

blood pressure on arrival was highly elevated, and her sister explained that Petitioner “ha[d] not 

taken any [blood pressure] med[ication] as she ran out last Friday.” Id. at 78. 

Petitioner underwent a head CT, which did not reveal “definite evidence of large acute 

intracranial hemorrhage,49 territorial infarction,50midline shift or mass effect.” Id. at 83. However, 

it did reveal some “minimal left frontal sulcal51 hyperdensity[,] which could be artificial.” Id.

Petitioner also underwent a brain MRI, which revealed “areas of abnormal T2/FLAIR signa1 

intensity seen predominantly in the subcortical white matter52 in the left posterior

temporal/occipital lobe region[,]53 as well as in the right occipital region, bilateral centrum 

48 Propofol is “a short-acting anesthetic and sedative used in induction and maintenance of general 

anesthesia and also for sedation . . . .” Propofol, DORLAND’S, https://www.dorlandsonline.com (last 

visited Feb. 2, 2021).

49 An intracranial hemorrhage is “bleeding within the cranium, which may be extradural, subdural, 

subarachnoid, or cerebral (parenchymatous)[.]” Intracranial Hemorrhage, DORLAND’S, 

https://www.dorlandsonline.com (last visited Feb. 3, 2021).

50 Infarction, or infarct, is “an area of coagulation necrosis in a tissue due to local ischemia resulting from 

obstruction of circulation to the area . . . .” Infarct, DORLAND’S, https://www.dorlandsonline.com (last 

visited Feb. 3, 2021). Ischemia is “deficiency of blood in a part . . . of a blood vessel.” Ischemia, 

DORLAND’S, https://www.dorlandsonline.com (last visited Feb. 3, 2021).

51 A sulcus is a “long groove or furrow, especially one of the cerebral sulci[,]” which are “the furrows on 

the surface of the brain between the cerebral gyri.” Sulcus, DORLAND’S, https://www.dorlandsonline.com 

(last visited Feb. 3, 2021); Cerebral Sulci, DORLAND’S, https://www.dorlandsonline.com (last visited Feb. 

3, 2021). Cerebral gyri are “the tortuous convolutions of the surface of the cerebral hemispheres, caused 

by folding of the cortex and separated by sulci.” Cerebral Gyri, DORLAND’S, 

https://www.dorlandsonline.com (last visited Feb. 3, 2021).

52 White matter, also known as white substance and substantia alba, is “the nervous tissue of the brain and 

spinal cord composed mostly of myelinated nerve fibers arranged in bundles (fasciculi).” Substantia Alba, 

DORLAND’S, https://www.dorlandsonline.com (last visited Feb. 3, 2021).

53 The temporal lobe is “the lower lateral lobe of the cerebral hemisphere . . . .” Lobus Temporalis, 

DORLAND’S, https://www.dorlandsonline.com (last visited Feb. 3, 2021). The occipital lobe is “the 

posterior portion of the cerebral hemisphere, on the medial surface extending from the posterior pole to 

the parietooccipital fissure but on the lateral surface continuous with the parietal lobe superiorly and with 

the temporal lobe inferiorly.” Lobus Occipitalis, DORLAND’S, https://www.dorlandsonline.com (last 

visited Feb. 3, 2021). The cerebral hemisphere is “either half of the cerebrum, “which is “the main portion 
13

semiovale, [and] left parietal region.” Pet’r’s Ex. 6(b) at 219. Doctors noted that, “[g]iven 

[Petitioner’s] clinical history, these findings are concerning for an etiology such as posterior 

reversible encephalopathy [(“PRES”)].

54” Id. Petitioner also underwent a psychiatric consultation 

on August 29, 2014. Id. at 216. The note reflects that Petitioner’s medical history was “significant 

for self[-]home[-]dialysis for ESRD apparantly [sic] sustained after a flu shot a year ago.” Id.

Petitioner “acknowledged depression ‘[ten percent] of the time’ and anxiety, related to her kidney 

malfunction requiring home dialysis and ultimately needing a . . . kidney transplant.” Id. Petitioner 

ultimately expressed that she “does not want or require psychiatric treatment[,]” and she 

“decline[d] recommendation measures that include psychotherapy and potential medication . . . .” 

Id. at 220. Petitioner was discharged from the hospital that day with a final diagnosis of PRES and 

a prescription for Dilantin.

55 Id. at 222.

On September 4, 2014, Petitioner presented to Dr. Swauger to follow up regarding her 

recent hospitalization. Pet’r’s Ex. 12 at 16. Petitioner reported “feeling okay” since discharge. Id.

She also reported being “a little swollen, but [was not experiencing any] further headaches.” Id.

She noted that she has not experienced any nausea, vomiting, or blurred vision, but she 

“[a]dmit[ted] that she still d[id] not have much of an appetite . . . .” Id. Petitioner’s examination 

was unremarkable, and Dr. Swauger directed her to follow up again in two months. Id.

Petitioner underwent a repeat brain MRI on October 2, 2014. Pet’r’s Ex. 6(b) at 200. The 

impression was “[i]nterval resolution of areas . . . previously seen [as] parenchymal signal 

abnormality[] compatible with resolution of PRES.” Id. In addition, there were “[n]o new lesions 

[seen] elsewhere in [Petitioner’s] brain.” Id. 

On October 10, 2014, Petitioner presented to the emergency room for a malfunctioning PD

catheter. Pet’r’s Ex. 4 at 5. She was released the same day. See id. at 7. Petitioner presented to Dr. 

Nayar for a follow-up on October 13, 2014, and reported that “[s]he has not been able to drain [her 

PD catheter] since last Thursday and has not had a complete dialysis [treatment] in [five] days.” 

Id. Dr. Nayar noted that Petitioner’s “PD site is [clean/dry/intact,]” and a “[workup] was negative 

of the brain, occupying the upper part of the cranial cavity.” Hemisphaerium Cerebri, DORLAND’S, 

https://www.dorlandsonline.com (last visited Feb. 3, 2021);

Cerebrum, DORLAND’S, https://www.dorlandsonline.com (last visited Feb. 3, 2021).

54 Posterior reversible encephalopathy syndrome, also known as reversible posterior leukoencephalopathy 

syndrome, posterior leukoencephalopathy syndrome, and posterior reversible leukoencephalopathy 

syndrome, is “a syndrome resulting from leukoencephalopathy with edema in posterior parts of the 

occipital and parietal lobes, characterized by headaches, confusion, seizures, and visual disturbances[.]” 

Reversible Posterior Leukoencephalopathy Syndrome, DORLAND’S, https://www.dorlandsonline.com (last 

visited Feb. 3, 2021). Leukoencephalopathy refers to “any group of diseases affecting the white matter of 

the brain, especially of the cerebral hemispheres, and occurring as a rule in infants and children.” 

Leukoencephalopathy, DORLAND’S, https://www.dorlandsonline.com (last visited Feb. 3, 2021). The 

parietal lobe is “the upper central lobe of the cerebral hemisphere . . . .” Lobus Parietalis, DORLAND’S, 

https://www.dorlandsonline.com (last visited Feb. 3, 2021).

55 Dilantin is a trademark for phenytoin, an anticonvulsant used to treat and prevent seizures and related 

disorders. Dilantin, DORLAND’S, https://www.dorlandsonline.com (last visited Feb. 3, 2021); Phenytoin, 

DORLAND’S, https://www.dorlandsonline.com (last visited Feb. 3, 2021).
14

for [p]eritonitis.56” Id. On exam, Dr. Nayar noted that Petitioner was “volume overloaded[,]” 

although she “state[d that] she is voiding a moderate [amount] on her current dose of Lasix 57. . . 

.” Id. Therefore, Dr. Nayar “advised [Petitioner] to go to the hospital for [hemodialysis (“HD”) 

cath[eter] placement so [they] could start [HD] . . . .” Id. However, Petitioner “refus[ed] to do so 

at [that] time[]” and noted that she had an appointment for an evaluation of her PD catheter the 

following day. Id. 

Petitioner reported again to the emergency room on October 15, 2015, “with complaints 

of abdominal pain, generalized fatigue, malaise[,] and diaphoresis.58” Pet’r’s Ex. 3(a) at 331. The 

note continues that, “[a]pparently, [Petitioner] ha[d] not received her scheduled [PD] due to 

malfunctioning of her [PD] catheter.” Id. Petitioner indicated that she “had a laparoscopic removal 

of [her PD] catheter scheduled . . . ; however, owing to her condition becoming worse[,] she 

presented to the [emergency room].” Id. While at the emergency room, Petitioner had a 

consultation with Dr. Nayar. Id. at 334–36. Dr. Nayar reviewed Petitioner’s medical history and 

noted that Petitioner was “on [the] active transplant list and [was] waiting for her sister to possibly 

donate a kidney.” Id. at 334. Dr. Nayar was concerned that Petitioner was suffering from 

peritonitis, and she conducted a draining procedure to procure fluid to culture. Id. at 335. Dr. Nayar 

also wrote that Petitioner would undergo “[HD] until [doctors could] evaluate the PD catheter to 

see if this modality can be continued.” Id. at 336. Petitioner underwent a successful HD catheter 

placement on that date. Pet’r’s Ex. 3(b) at 97. Petitioner was ultimately diagnosed with peritonitis 

and prescribed Vancomycin59 and Zosyn.

60 Pet’r’s Ex. 3(a) at 339. She was discharged on October 

17, 2014. Id. at 318. 

On October 22, 2014, Petitioner presented to Dr. Swauger for a follow-up. Pet’r’s Ex. 12 

at 11. Petitioner reported that she was “currently receiving the antibiotics while on HD[]” and was 

“going to HD on [Monday/Wednesday/Friday].” Id. Petitioner further stated that “[s]he ha[d] not 

had any further seizures[] and [was] weaning off of the [seizure] medication.” Id. Dr. Swauger 

recommended that Petitioner receive the Hepatitis A/B, flu, and pneumovax vaccines, but 

Petitioner declined. Id. at 12. Dr. Swauger noted that Petitioner was “tolerating HD much better 

than [PD].” Id. 

56 Peritonitis is “inflammation of the peritoneum, with exudations of serum, fibrin, cells, and pus . . . .” 

Peritonitis, DORLAND’S, https://www.dorlandsonline.com (last visited Feb. 2, 2021). 

57 Lasix is a trademark for furosemide, “a loop diuretic used in the treatment of edema associated with 

congestive heart failure or hepatic or renal disease, as an adjunct in the treatment of acute pulmonary 

edema, and in the treatment of hypertension . . . .” Lasix, DORLAND’S, https://www.dorlandsonline.com 

(last visited Feb. 2, 2021).

58 Diaphoresis is another word for sweating. Diaphoresis, DORLAND’S, https://www.dorlandsonline.com 

(last visited Feb. 2, 2021).

59 Vancomycin hydrochloride is an antibiotic. Vancomycin Hydrochloride, DORLAND’S, 

https://www.dorlandsonline.com (last visited Feb. 2, 2021).

60 Zosyn is a trademark for a combination of piperacillin sodium and tazobactam sodium, which are used 

to treat infections. Zosyn, DORLAND’S, https://www.dorlandsonline.com (last visited Feb. 2, 2021); 

Piperacillin Sodium, DORLAND’S, https://www.dorlandsonline.com (last visited Feb. 2, 2021); Nephritis, 

DORLAND’S, https://www.dorlandsonline.com (last visited Feb. 2, 2021); Tazobactam Sodium, 

DORLAND’S, https://www.dorlandsonline.com (last visited Feb. 2, 2021).
15

Petitioner had an AV fistula61 placed in her left arm by Gene W. Manzetti, M.D., on 

November 20, 2014. Pet’r’s Ex. 10 at 18. At follow-up appointments with Dr. Manzetti on January 

12 and February 9, 2015, Dr. Manzetti noted that Petitioner’s fistula was “showing some 

maturation” but also noted that Petitioner “does have a lot of venous tributaries over her forearm.” 

Id. at 6–7. On March 9, 2015, Petitioner’s fistula was declared “occluded[,]” and Dr. Manzetti 

wrote that “the plan will be to have [Petitioner] undergo creation of a higher AV fistula.” Id. at 5. 

Petitioner underwent a successful placement of an AV fistula in her upper left arm on March 17, 

2015. Id. at 2. 

III. Experts

A. Expert Review

1. Petitioner’s Expert, M. Eric Gershwin, M.D.

Dr. Gershwin received his medical degree from Stanford University in 1971. Pet’r’s Ex. 

20 at 1. He is licensed to practice in California and holds board-certifications in internal medicine, 

internal medicine with a subspecialty in rheumatology as well as allergy and clinical immunology. 

Id. at 2. Dr. Gershwin’s clinical experience includes serving as the Chief of the Division of 

Rheumatology/Allergy and Clinical Immunology at the University of California School of 

Medicine, Davis since 1982. Id. He also has academic experience, including serving as the Jack 

and Donald Chia Professor of Medicine within the Division of Rheumatology/Allergy and Clinical 

Immunology at the University of California, Davis and as a Distinguished Professor of Medicine 

within the same division. Id. at 1. Dr. Gershwin’s curriculum vitae includes numerous books, book 

chapters, and research papers of which he is a listed author. See id. at 8–125. 

During his testimony, Dr. Gershwin stated that he has experience with treating patients 

with kidney diseases, but he also noted that he “do[es] not have significant experience” treating 

patients with FGN and estimated that he “perhaps [had] seen one or two [FGN] patients” during 

his entire career. See Tr. 54:23–55:12. In response to my questioning, Dr. Gershwin stated that 

neither his research nor his publications involved FGN, although he has conducted research on 

nephritis, which he described as being “mostly related to lupus[,]” and on “other autoimmune 

kidney diseases . . . .” Tr. 56:18–57:4. 

Dr. Gershwin submitted two expert reports and testified at the entitlement hearing. See

Pet’r’s Exs. 19, 49; Tr. 51:1–106:23, 167:1–168:7. At Petitioner’s request, and without objection 

from Respondent, I admitted Dr. Gershwin to testify as an expert in internal medicine, 

rheumatology, and immunology. Tr. 56:9–16.

2. Petitioner’s Expert, Wesam F. Ballouk, M.D.

61 AV fistula refers to a “passage[ that] may be . . . created surgically for arteriovenous access . . . .” 

Fistula, DORLAND’S, https://www.dorlandsonline.com (last visited Feb. 2, 2021); see also AV, 

DORLAND’S, https://www.dorlandsonline.com (last visited Feb. 2, 2021).
16

Dr. Ballouk received his medical degree from Damascus University in 1996. Pet’r’s Ex. 18 

at 1. He completed an internship in psychiatry/internal medicine and a residency in internal 

medicine at the University of Tennessee Health Science Center in 2000 and 2002, respectively. Id.

Dr. Ballouk also completed a post-residency fellowship in nephrology at the same institution in 

2005. Id. He is licensed to practice medicine in both Tennessee and Arkansas, and he is boardcertified in both internal medicine and nephrology. Id. at 2; Tr. 175:25–176:2. Dr. Ballouk’s 

clinical experience includes serving as the Chairman of the Nephrology Division in the Internal 

Medicine Department at Saint Francis Hospital in Bartlett, Tennessee since 2006. Id. Also 

beginning in 2006, Dr. Ballouk has served as the Medical Director of multiple HD units in 

Tennessee, and in 2013, Dr. Ballouk began serving as the Medical Director of a home dialysis unit. 

Id. Dr. Ballouk also has academic experience, including serving as an Assistant Professor of 

Internal Medicine at the University of Tennessee Health Science Center from 2007 to 2015. Id. 

Dr. Ballouk submitted two expert reports and testified at the entitlement hearing. See

Pet’r’s Exs. 18, 50; Tr. 174:20–283:25, 388:16–402:7. At Petitioner’s request, and without 

objection from Respondent, I admitted Dr. Ballouk to testify as an expert in internal medicine and 

nephrology. Tr. 177:15–20.

3. Respondent’s Expert, Arnold Levinson, M.D.

Dr. Levinson received his medical degree from the University of Maryland in 1969. 

Resp’t’s Ex. D at 1. He is licensed to practice medicine in Pennsylvania and is board -certified in 

internal medicine and allergy and clinical immunology. Id. at 2–3. Dr. Levison has extensive 

academic and practical experience, although he retired in 2014. He served as a Professor of 

Medicine and Neurology at the University of Pennsylvania School of Medicine from 1994 to 2009, 

and as an Associate Director of Undergraduate Medical Education at the same institution from 

1997 to 1999. Id. at 2. His clinical experience includes serving as the Chief of the Allergy and 

Immunology Section within the Pulmonary, Allergy, and Critical Care Division at the University 

of Pennsylvania School of Medicine from 1998 to 2009. Id. He also served as the Chief of Allergy 

and Immunology at the Philadelphia Veterans Administration Medical Center from 1999 –2007. 

Id. His curriculum vitae includes numerous publications and editorials of which he is a listed 

author. See id. at 10–21. 

Since his retirement in 2014, Dr. Levinson explained that he, among other responsibilities, 

“still maintain[s] a significant amount of activity . . . at [the University of Pennsylvania] . . . in the 

teaching arena, particularly teaching and mentoring fellows, and to some extent residents . . . .” 

Tr. 109:17–24. Prior to his retirement, Dr. Levinson estimated that “about [twenty] percent[]” of 

his time was devoted to patient care, mainly those “who suffered from complex allergic 

autoimmune . . . and/or immunodeficiency disorders.” Tr. 110:12–21.

Dr. Levinson submitted one expert report and testified at the entitlement hearing. See 

Resp’t’s Ex. C; Tr. 107:23–163:6. AtRespondent’s request, and without objection from Petitioner, 

I admitted Dr. Levinson to testify as an expert in immunology and clinical immunology . Tr. 

113:19–23.

4. Respondent’s Expert, Derek M. Fine, M.D.
17

Dr. Fine received his medical degree from the Johns Hopkins University School of 

Medicine in 1994. Resp’t’s Ex. B at 1. He completed his internship and residency at the Johns 

Hopkins Hospital/University School of Medicine from 1994 to 1997, and a fellowship in 

nephrology at the same institution from 1997 to 1999. Id. at 2. He currently holds both academic 

and clinical positions. Id. at 1. Beginning in 2008, he has served as an Associate Professor of 

Medicine at the Johns Hopkins University School of Medicine, and since 2009, he has served as 

the Fellowship Director within the Division of Nephrology at the same institution. Id. Beginning 

in 2014, Dr. Fine has served as the Medical Director at Johns Hopkins Davita – Bond Street 

Dialysis Unit. Id. His curriculum vitae includes numerous publications of which he is a listed 

author. See id. at 2–10. Dr. Fine estimated that he spends five to fifteen percent of his time on 

research, depending on the year. Tr. 289:19–22.

Dr. Fine explained during his testimony that his work involves diagnosing patients at all 

stages of various renal diseases, and that he has seen “probably around four or five[]” patients with 

FGN throughout his career. Tr. 290:25–291:10. Dr. Fine also noted that he has experience in 

pathology, which he described as “sort of [an] ongoing education in pathology [whereby he] 

frequently look[s] at pathology with [the] pathologists [at Johns Hopkins] and discuss[es] the 

findings and the implications [of biopsies and pathology reports,] and [therefore he has] a fairly 

solid base of . . . nephropathology.” Tr. 291:11–292:5.

Dr. Fine submitted two expert reports and testified at the entitlement hearing. SeeResp’t’s 

Exs. A, E; Tr. 284:19–387:23. At Respondent’s request, and without objection from Petitioner, I

admitted Dr. Fine to testify as an expert in nephrology. Tr. 292:6–9. 

B. Expert Reports and Testimony

1. Petitioner’s Expert, Dr. Gershwin

Dr. Gershwin stated that his theory was that the flu vaccine “exacerbated [Petitioner’s] 

ongoing FGN.” Tr. 58:3–4. Specifically, Dr. Gershwin wrote that his theory was “that the cytokine 

response following the [flu] vaccination would have accelerated [Petitioner’s] [GN] and made it 

worse. In other words, she went from the onset of a renal disease to requiring dialysis at a more 

rapid rate than one would anticipate.” Pet’r’s Ex. 19 at 1. He explained that he built his theory on 

two assumptions. First, Dr. Gershwin assumed “that the time of onset of [Petitioner’s] FGN was 

about the same time, [or] certainly preceded the [flu] vaccination.” Tr. 58:6–8. He noted that “if 

the time of [FGN] onset was distant from the vaccination, then [he] would not hold” the opinion 

that the flu vaccine exacerbated Petitioner’s FGN. Tr. 58:8–9. Dr. Gershwin stated that “[i]f this 

disease started six months before the vaccination[,]” he would not hold his opinion or offer it. Tr.

83:2–4. He indicated that his opinion was based on onset “certainly within a window of six weeks 

before the vaccine.” Tr. 83:9–10. Second, Dr. Gershwin “assumed that [Petitioner’s] FGN was 

worse than what one would expect in an individual of her age with FGN.” Tr. 58:10–12. Again, 

Dr. Gershwin noted that “if there’s evidence and the Court is convinced that the natural history of 

her FGN was the same as you would expect of another cohort of patients with FGN, then [he] 

would not be here.” Tr. 58:12–15. 
18

During his testimony, Dr. Gershwin discussed cytokines in detail. He explained that “a 

cytokine is a low molecular weight material produced by a whole variety of cells in the body.” Tr. 

61:6–7. He noted that “[v]irtually any cell can produce some form of cytokine, or a chemokine or 

what’s often called its cognizant receptor,” and explained that they are “a way to signal or activate 

cells. [Cytokines] allow[] cells to talk to each other.” Tr. 61:8–11. He stated that cytokines 

“facilitate[] the immune response, amplif[y the] immune response.” Tr. 62:19–20. He further

stated that cytokine signaling can affect cell behavior in a multitude of ways, the effectiveness of 

which “will depend on the health of the cell . . . .” Tr. 64:2–7. He provided the following example

of how cytokines can affect cell behavior: “a very simple example is [a cytokine] can make cells 

divide. It can make cells go through autophagy, which is a form of how cells die . . . .” Tr. 64:5–

11. Dr. Gershwin further testified that cytokines are involved in both the innate and adaptive 

immune systems, and that doctors “classically . . . divided cytokines into what are called Th1 and 

Th2 responses, [or] those that promote inflammation and those that inhibit inflammation.” Tr. 

62:24–63:7. 

Dr. Gershwin also opined that cytokines can act both locally and systemically. Tr. 66:8–

16. He cited to an article by Ortega and Fornoni to support this proposition. Tr. 65:3–66:7; Pet’r’s 

Ex. 57.62 The authors of this article conducted a literature review to “provide a general 

comprehensive overview of the role of the main cytokine families in the setting of [acute kidney 

injury], CKD, [end stage kidney disease], [GN], and transplantation, and to explore their 

relationship to clinical outcomes, mortality, and recovery of renal function.” Pet’r’s Ex. 57 at 2. 

They noted that “cytokines may act in a systemic, paracrine, or an autocrine fashion.” Id. at 1. Dr. 

Gershwin provided further explanation of these terms. He explained that “systemic” means that 

“cytokines that are produced elsewhere [in the body] . . . can act at a distant site [elsewhere in the 

body].” Tr. 65:16–17. He further explained that “paracrine” refers to “a cell-to-cell interaction,” 

whereas “autocrine” refers to “an individual cell [that] secretes cytokines and then the cytokines 

will feed back and impact its own cell.” Tr. 65:19–66:1. Dr. Gershwin affirmed that the “key 

takeaway” from this article is the discussion of the different ways that cytokines can act on a cell. 

Tr. 66:8–11. During his testimony, he noted that “in this case, we’re really referring to systemic.” 

Tr. 66:11–12. Dr. Gershwin testified, however, that “these [types of action] overlap.” Tr. 66:12–

13. The article concludes by noting that currently available studies on cytokines “do not provide 

any evidence for a causative role of a given cytokines in disease pathogenesis or progression.” 

Pet’r’s Ex. 57 at 12. 

In his first expert report, Dr. Gershwin wrote that “[t]he role of cytokines in the activity of 

the immune mediated/inflammatory renal disease has been the subject of intense study for more 

than [twenty] years.” Pet’r’s Ex. 19 at 2. He cited to a study by Niemer et al., the data of which 

Dr. Gershwin described as “confirmatory of earlier work that there is a contribution of both proinflammatory and anti-inflammatory cytokines63 by renal cells that contribute to the natural history 

62 Luis M. Ortega & Alessia Fornoni, Role of Cytokines in the Pathogenesis of Acute and Chronic Kidney 

Disease, Glomerulonephritis, and End-stage Kidney Disease, 2 INTERN.J. OF INTERFERON, CYTOKINE 

AND MEDIATOR RESEARCH 49 (2010).

63 Cytokine is “a generic term for nonantibody proteins released by one cell population . . . on contact 

with a specific antigen, which act as intercellular mediators, as in the generation of an immune response.” 

Cytokine, DORLAND’S, https://www.dorlandsonline.com (last visited Feb. 2, 2021).
19

of disease.” Id.; Pet’r’s Ex. 52.64 In this study, the authors “examined the in situ expression of 

[interleukin (“IL”)]-1065 and [tumor necrosis factor (“TNF”)66]-α in renal biopsy specimens from 

patients with different forms of GN and variable clinical presentations.” Id. at 2. They found “that 

resident renal cells are the major source of TNF-α and IL-10.” Id. at 12. They “propose[d] that 

TNF-α is involved in the pathogenesis of interstitial fibrosis, . . . [whereas the] excessive 

production [of IL-10] seems to be associated with active and/or progressing glomerular lesions.” 

Id. The authors concluded that their study “confirm[s] previous suggestions that pro[-

]inflammatory and anti[-]inflammatory cytokines are produced in situ by resident renal cells and 

contribute to the natural course of human GN.” Id. at 1.

Dr. Gershwin opined that “[a] vaccine would not work unless it produced cytokines.” Tr. 

61:13–14. Dr. Gershwin cited to a paper by Morel and Turner to support this proposition. Tr. 

61:17–62:9; Pet’r’s Ex. 56.67 The authors conducted a “review [that] focus[es] on recent advances 

in the ways [dendritic cells]68 and cytokines can be used to develop the most appropriate and 

effective vaccines.” Pet’r’s Ex. 56 at 1. When discussing cytokines, the authors wrote that 

“[c]ytokine production . . . plays an important role in defining the type of T cell effector response 

that is induced.” Id. at 2. They concluded that “[dendritic cells] and the cytokines they produce 

play a key role in driving . . . immune responses and can be harnessed to induce an effective 

immune response against the pathogen or disease of choice.” Id. at 7–8. Dr. Gershwin testified that 

this article “emphasiz[es] that in producing vaccines, the measurement of cytokines is basically 

the gold standard, meaning when you’re trying to design a vaccine, one way to predict how optimal 

it is [by] how good of a cytokine response it produces.” Tr. 62:10–16.

When discussing the flu vaccine generally, Dr. Gershwin testified that it triggers the 

production of cytokines. Tr. 67:14–16. He explained that the types of cytokines produced by the 

flu vaccine in “individuals will be different, and they’ll be different by age, but some of the key 

[cytokines produced by the flu vaccine] are interferon family, IL-2, IL-5, IL-10, IL-17, IL-21. 

64 Zofia I. Niemir et al., In Situ Upregulation of IL-10 Reflects the Activity of Human 

Glomerulonephritides, 32:1 AM.J. OF KIDNEY DISEASES 80 (1998). 

65 Interleukin-10 is “a cytokine produced by activated macrophages, certain lymphocytes, and other cells 

that decreases both innate and T cell-mediated immune inflammation[.]” Interleukin-10, DORLAND’S, 

https://www.dorlandsonline.com (last visited Feb. 2, 2021).

66 Tumor necrosis factor refers to “either of two lymphokines that are capable of causing in vivo 

hemorrhagic necrosis of certain tumor cells but not affecting normal cells[.]” Tumor Necrosis Factor, 

DORLAND’S, https://www.dorlandsonline.com (last visited Feb. 2, 2021). Lymphokines are “soluble 

cytokine[s] that mediate[] immune responses[]” that are “released by sensitized lymphocytes on contact 

with antigen.” Lymphokine, DORLAND’S, https://www.dorlandsonline.com (last visited Feb. 2, 2021).

Lymphocytes are “any of the mononuclear, nonphagocytic leukocytes, found in blood, lymph, and 

lymphoid tissues, that are the body’s immunologically competence cells and their precursors.” 

Lymphocyte, DORLAND’S, https://www.dorlandsonline.com (last visited Feb. 2, 2021). Leukocytes are 

white blood cells, “colorless blood cell[s] capable of ameboid movement[.]” Leukocyte, DORLAND’S, 

https://www.dorlandsonline.com (last visited Feb. 3, 2021).

67 Penelope A. Morel & Michael S. Turner, Designing the Optimal Vaccine: The Importance of Cytokines 

and Dendritic Cells, 3 OPEN VACCINE J. 7 (2010).

68 Dendritic refers to dendrites, which are “threadlike extensions of the cytoplasm of a neuron . . . .” 

Dendritic, DORLAND’S, https://www.dorlandsonline.com (last visited Feb. 2, 2021); Dendrite, 

DORLAND’S, https://www.dorlandsonline.com (last visited Feb. 2, 2021).
20

Lots of other ones as well.” Tr. 67:17–23. Dr. Gershwin stated that cytokines produced by the flu 

vaccine “help facilitate the immune response, they will act on cells, they will amplify them, so in 

effect cell differentiation, [and] would promote inflammation.” Tr. 68:20–24. He continued, 

“[t]hey will make an ongoing inflammation get worse,” depending on “the window of opportunity” 

of when the vaccine is administered. Tr. 68:25–69:2. When asked whether “cytokines that are 

produced in a host following a vaccine[] . . . travel around the body,” Dr. Gershwin responded that 

“they do get in the sera, and they do have a sera half[-]life. And the antigen [in the vaccine] will 

be systemic as well, but it’s really in the sera cytokines that will affect, in a systemic way, 

peripheral cells as well.” Tr. 69:3–10. He further explained that the cytokines “get around the body 

because you can measure them in circulation.” Tr. 69:11–12. Dr. Gershwin also opined that these 

cytokines would interact with the kidneys, “[p]articularly . . . if . . . [the vaccination occurs in] the 

early phase of [Petitioner’s kidney] disease.” Tr. 70:1–5. 

Dr. Gershwin also discussed FGN during his testimony, although he noted that he “will 

defer to [the] nephrologists” on FGN-specific topics. Tr. 70:8–9. He described FGN as “an 

enigmatic form of [GN]. [It is an e]nigmatic form of kidney inflammation, and there are these . . . 

filaments that are deposited, they’re very small, they stain. We don’t know that much about it.” 

Tr. 70:9–13. Dr. Gershwin referred to FGN as an immunological disease, and he cited to an article 

by Rosenstock and Markowitz for support. Tr. 70:24–72:6; Pet’r’s Ex. 55.69 The authors of this 

paper wrote that “[t]he fibrils that characterize FGN are predominantly confined to the glomeruli 

and stain intensely by IF for IgG, C3, κ, and λ, strongly suggesting that the fibrils are composed 

of a complex of antibodies and antigens.” Pet’r’s Ex. 55 at 1. They continue, “[t]he absence of 

staining for Congo red (with rare exception) and the composition of the fibrils help to differentiate 

FGN from amyloidosis,70 while the diameter of the fibrils and the absence of a microtubular 

appearance with a hollow core help differentiate FGN from immunotactoid glomerulopathy.71” Id.

Dr. Gershwin testified that this passage suggests that FGN is an immunological disease, as the 

authors “even use the word immunotactoid, in the next to last word of that [passage]. But there is 

still a wide gap in knowledge.” Tr. 71:24–72:6. 

When asked whether cytokines played a role in pathogenesis of FGN, Dr. Gershwin stated 

that “cytokines play a role in [GN]. As far as [he] know[s] . . . there is nobody who has studied 

cytokine biology in FGN.” Tr. 72:7–11. He explained that this lack of a definitive answer stems 

from FGN being “uncommon, [and he] suspect[s] people don’t have enough patients in one series 

to be able to do those sorts of intensive studies . . . . There haven’t been evidence-based, doubleblind studies, as there have been in lupus nephritis72[, for example.] So[,] there is this gap.” Tr. 

72:14–24. However, Dr. Gershwin stated he “would still argue that proof of principle analogy that 

69 Jordan L. Rosenstock & Glen S. Markowitz, Fibrillary Glomerulonephritis: An Update, 4 KIDNEY INT.

REP. 917 (2019). 

70 Id.

71 Immunotactoid glomerulopathy is “a type of fibrillary glomerulonephritis having particularly large 

fibrils (immunotactoids). Immunotactoid Glomerulopathy, DORLAND’S, https://www.dorlandsonline.com 

(last visited Feb. 2, 2021).

72 Lupus nephritis is “glomerulonephritis (diffuse, focal, or membranous) associated with systemic lupus 

erythematosus, marked by deposition of antigen-antibody complexes in the mesangium and basement 

membrane.” Lupus nephritis, DORLAND’S, https://www.dorlandsonline.com (last visited Feb. 3, 2021). 
21

cytokine biology, as with any other form of inflammation, would play a critical role.” Tr. 72:25–

73:2. 

Dr. Gershwin testified that he “[a]bsolutely” recommends the flu vaccine to his patients. 

Tr. 75:16–18. Dr. Gershwin further testified that he would recommend the flu vaccine to his 

patients that have kidney disease “if they aren’t in the early phase” of the disease. Tr. 75:19–20. 

He explained that “some of the best studies that have been done on vaccination are done in people 

with established disease.” Tr. 76:3–5. He further explained this distinction by comparing patients 

with “ongoing” disease, like lupus and rheumatoid arthritis [(“RA”)],

73 with patients that have an 

acute onset of kidney disease. Tr. 75:22–77:2. Dr. Gershwin testified that lupus and rheumatoid 

arthritis have “latency time[s] . . . measured in years. So[,] if [he] see[s] a patient in [his] clinic 

and [he’s] about to start the biologics, [he] will vaccinate them, but . . . their disease . . . probably 

began [five] or [ten] years earlier.” Tr. 76:2–10. He further explained that doctors “can find 

evidence of antibodies in the blood in rheumatoid arthritis and even lupus patients many, many 

years before they ever get clinical symptomatology.” Tr. 76:10–13. Therefore, he would vaccinate 

these types of patients. Tr. 76:2. 

However, Dr. Gershwin stated that that is “a different scenario than comparing the safety 

of vaccines in somebody . . . just beginning the throws of an acute renal process[,] which involves 

inflammation.” Tr. 76:21–24. He wrote that “[t]he basis for concern regarding administration of 

[the flu] vaccine in an active inflammatory response is the altered immune profile and, in 

particular, the cytokine response that is produced following vaccination.” Pet’r’s Ex. 19 at 3. He 

explained that the “[flu] vaccine elicits a rigorous cytokine response and this response begins 

within hours of the vaccination.” Id. He further explained that “[t]his [inflammatory response] 

would have significantly aggravated any underlying inflammation, including and, in particular, 

[Petitioner’s] pre[-]existing [FGN].” Pet’r’s Ex. 49 at 1. 

Dr. Gershwin explained that the flu vaccination “accelerated [Petitioner’s] kidney disease.” 

Tr. 79:18. He affirmed that Petitioner would have been at risk for exacerbation by the flu vaccine 

“[i]f . . . [Petitioner] was in the early phases of [her] disease[]” when she was vaccinated. Tr. 78:2–

6. If this was the case, then Dr. Gershwin believes that Petitioner “was a susceptible host because 

she was in the initial phases of her active kidney disease.” Tr. 79:15–16. In this scenario, he 

explained that:

[the flu vaccine] would have led to upregulation of multiple cytokines, including 

pro-inflammatory cytokines, which . . . would exacerbate an ongoing inflammatory 

process in the kidney, both from a systemic perspective, . . . cytokines coming in 

affectingcells, which might affect those cells both in a paracrine and in an autocrine 

fashion. 

Tr. 78:16–22. 

73 Rheumatoid arthritis is “a chronic systemic disease primarily of the joints, usually polyarticular, 

marked by inflammatory changes in the synovial membranes and articular structures and by muscle 

atrophy and rarefaction of the bones.” Rheumatoid Arthritis, DORLAND’S, 

https://www.dorlandsonline.com (last visited Feb. 2, 2021).
22

Prior to receiving the flu vaccine at issue, Dr. Gershwin stated that Petitioner had not been 

diagnosed with or treated for nephritis. Tr. 73:13–16. Dr. Gershwin nonetheless opined that 

Petitioner “was suffering from it at the time of her vaccin[ation],” although he was “really bas[ing]

that on the nephrologist.” Tr. 73:20–23. He continued that nephrologists “have an opinion about 

that . . . , which helps [them] to come to that [opinion], and that is that the nausea that people 

experience from renal failure often is more dependent on the rate of rise of BUN in the absolute 

amount.” Tr. 73:22–74:1. He further explained that “somebody with acute renal failure in which 

there's a . . . rise in BUN[] is more likely to experience nausea.” Tr. 74:5–8. However, Dr. Gershwin 

again stated that he would defer to a nephrologist” when asked whether he had an opinion as to 

the onset date of Petitioner’s FGN. Tr. 74:15–18. 

Dr. Gershwin discussed the harm caused by Petitioner’s flu vaccine by citingto Petitioner’s 

biopsy results. Dr. Gershwin identified the “extensive inflammation” present, which he noted was 

“critical to [his] opinion because inflammation is never helpful, even in most infectious diseases. 

It can be harmful.” Tr. 80:21–24. He also identified the following line in the biopsy report as 

significant to his opinions: “The interstitial infiltrates contain mostly mononuclear cells.” Tr. 

81:11–12 (quoting Pet’r’s Ex. 3 at 96). Dr. Gershwin described “mononuclear cells, or

monocytes,” as “professional antigen-presenting cells[]” that “would be particularly susceptible to 

cytokines.” Tr. 81:14–15. He also referenced “the one giant cell,” which he described as

“consistent with an immune inflammatory response.” Tr. 81:22–82:2. 

Although Dr. Gershwin wrote, “it is unknown what the actual date of onset of [Petitioner’s 

GN] is,” he noted that, “it is clear that there was significant exacerbation in the beginning of 

November 2013, which culminated in the hospitalization on November 21, 2013.” Pet’r’s Ex. 19 

at 3. Dr. Gershwin disagreed that Petitioner’s symptoms during this hospitalization were caused 

by a gastrointestinal illness, as suggested by Respondent, because “[t]here wasn't anyone else who 

was sick at the time, there wasn't any blood, there wasn't a history of food poisoning . . . .” Tr. 

83:24–84:4. Dr. Gershwin also noted that none of Petitioner’s treaters diagnosed her with a 

gastrointestinal illness during this time. Tr. 84:11–14. In addition, Dr. Gershwin thought that 

Petitioner’s “symptoms [during her hospitalization] would be consistent with acute renal failure. 

The nausea, the vomiting, the abdominal pain on exam was said to be mild, but it would be 

consistent with someone who’s vomiting.” Tr. 84:2–6. Dr. Gershwin further opined that diarrhea, 

which Petitioner also experienced, “can be present with acute renal failure.” Tr. 84:7–8. 

In addition, Dr. Gershwin testified that he “couldn’t find any[]” other aggravating factor 

for Petitioner’s FGN other than the flu vaccine. Tr. 84:14–18. He disagreed that Petitioner’s use 

of prescription pain medication played a role in her disease course, noting that “there was no 

concurrent evidence of liver disease[, which] one would have expected such a feature in many 

patients.” Pet’r’s Ex. 19 at 3. He testified that Petitioner “showed no signs of liver toxicity[]” 

despite being “on [the pain medication] for a long time.” Tr. 82:13–14. Dr. Gershwin also wrote

that “there is no literature to support the induction of [FGN] with pain medication.” Pet’r’s Ex. 19 

at 3. 

Dr. Gershwin concluded his first expert report by writing that he “would not have 

recommended vaccination on September 23, 2013,” because Petitioner was in the acute process of 
23

her FGN. Id. However, Dr. Gershwin further wrote that he does “not have any concern about 

vaccinating her now. In other words, her kidney disease is essentially burned out and she is 

dependent on dialysis.” Id. Therefore, he does “not envision a problem for further vaccination in 

people with stable renal failure.” Id. However, on cross-examination, Dr. Gershwin testified that 

he “would ask . . . a nephrologist” as to when Petitioner’s disease burned out. Tr. 93:23 –94:1. Dr. 

Gershwin clarified that he made his statement regarding vaccinating Petitioner now “only to 

explain . . . that [he] had no problem about vaccinating people with [ESRD] or longstanding 

autoimmune disease.” Tr. 94:4–7.

In response to my questioning, Dr. Gershwin explained that the inflammation stays in 

Petitioner’s kidneys because there’s “already . . . an early ongoing inflammatory process going on, 

which is immunologic, and then the cytokines would work there, produce harm . . . . It’s like a 

wound that [the cytokines are] exacerbating.” Tr. 100:3–7. He disagreed that Petitioner had 

inflammation in other parts of her body, namely her intestine and arm, noting that “ the intestine 

was just the symptom of the elevated BUN and the nausea from renal failure.” Tr. 100:8–14. He 

opined that “if you do a biopsy, there was no colitis, no ulcerative colitis, no inflammatory

gastroenteritis . . . . [A]t the [vaccination] site, there was some marker inflammation, and yes, that 

is part of the immune response to the vaccine . . . . [B]ut [he doesn’t] think it played any role in 

systemic disease.” Tr. 100:16–22. He continued, “[a]nd because there wasn't already an ongoing 

disease going on there, there's nothing for [the vaccine] to exacerbate.” Tr. 100:22–24. 

2. Petitioner’s Expert, Dr. Ballouk

Dr. Ballouk submitted two expert reports in this case. In his first report, Dr. Ballouk wrote 

that he “agree[s] that [Petitioner] has rapidly progressing [FGN,]” which he described as an

“inflammatory disease.” Pet’r’s Ex. 17 at 2. He opined that Petitioner “was likely suffering from 

nephritis at the time of her vaccination . . . , but she did not have any clinical manifestations of 

nephritis at that time.” Id. Dr. Ballouk wrote that “[i]t is possible that vaccination accelerated and 

made [Petitioner’s] nephritis worse[,]” and if it did, he argued that “the timing was appropriate 

given her hospitalization in November 2013 with renal insufficiency, which was likely the first 

clinical manifestation of her nephritis.” Id. Dr. Ballouk noted that “[i]t is [his] opinion that [the] 

flu vaccin[e] can produce an immune response[,] which includes cytokine production[;]” however, 

Dr. Ballouk also wrote that “the opinions of an immunologist would be helpful[]” in determining 

“whether it is more likely than not that [Petitioner’s] vaccination did aggravate her nephritis . . . .” 

Id. Aside from a brief factual background on Petitioner’s clinical course, Dr. Ballouk did not 

provide any additional information in his first expert report. See id. at 1–2. 

During his testimony, Dr. Ballouk expanded upon the points he discussed in his first expert 

report. Dr. Ballouk described GN as “inflammation of the glomeruli, which is the filtering part of 

the nephron74 in the kidneys. Each kidney has millions of nephrons, and if there’s any 

74 The nephron is “the anatomical and functional unit of the kidney, consisting of the renal corpuscle, the 

proximal convoluted tubule, the descending and ascending limbs of the loop of Henle . . . and the 

collecting tubule.” Nephron, DORLAND’S, https://www.dorlandsonline.com (last visited Feb. 3, 2021). 

The renal corpuscle is “a body that forms in the beginning of a nephron, consisting of a glomerulus 

surrounded by the glomerular capsule (an expanded portion of the renal tubule). Renal Corpuscle, 

DORLAND’S, https://www.dorlandsonline.com (last visited Feb. 3, 2021). The proximal convoluted tubule 
24

inflammation of the glomeruli, that will affect the function of the kidney.” Tr. 183:1–7. He stated 

that there are multiple causes of GN, including immune diseases, vasculitis, or nephrotic 

syndrome. Tr. 183:8–12. He also stated that GN “can cause renal failure.” Id. 

Dr. Ballouk described FGN as “one rare kind of [GN].” Id. He noted that “the exact cause 

is not yet known[,]” although he explained that “there are some coexisting factors found in the 

literature, like . . . [ten] to [twelve] percent [of FGN patients] have [an] autoimmune disease, like 

lupus.” Tr. 184:17–21. He also listed “[H]epatitis C” and “malignancy” as other coexisting factors. 

Tr. 184:20–21. Dr. Ballouk stated that FGN is a “little bit closer to an immune disease, so [it is] 

treat[ed] with immunosuppressants . . . [and] Prednisone.75” Tr. 184:22–185:1. He explained that 

FGN is thought of as an immune disease because “[t]here are new research studies showing that 

[FGN] is more like an inflammation with antibodies presented in the kidneys, . . . called DNAJB. 

That will tell me that there is acute inflammation of the kidneys. . . . [I]t’s kind of similar to 

autoimmune disease, like we see in lupus, and that will make me feel that . . . immunosuppressant 

medications will help in this kind of disease.” Tr. 185:2–13. 

Dr. Ballouk testified that FGN is “usually diagnosed by biopsy.” Tr. 183:24–25. He 

explained that “[f]irst . . . , the nephrologist will suspect [that] the patient [has GN] from the 

symptoms[,]” which he described as “swelling, sometimes feeling bad like nausea. All the 

symptoms of renal insufficiency and proteinuria.” Tr. 185:15–21. In addition, Dr. Ballouk

explained that many patients will complain of “foamy urine, . . . and a urine test . . . [will] find that 

they have a lot of protein or blood in the urine.” Tr. 185:21–22. He continued, “[t]hen [doctors 

will] do . . . blood work[,] which shows . . . BUN and creatinine . . . rising, so [doctors] will send 

[the patient] for a kidney biopsy . . . .” Tr. 185:23–25. Dr. Ballouk noted that FGN is “very hard 

to diagnose . . . without a biopsy.” Tr. 183:25–184:1. 

During his testimony, Dr. Ballouk discussed the results of Petitioner’s kidney biopsy. Tr. 

196:10–199:16. Dr. Ballouk stated that the biopsy results showed that Petitioner “had [FGN] for 

sure, with interstitial nephritis and focal global glomerulosclerosis and some extensive fibular 

atrophy.” Tr. 199:21–24. He continued, “looking at live microscope, that will also tell [a doctor] 

that [Petitioner] has some meningeal infiltrations with few nuclear cells.” Tr. 196:24–197:1. Dr. 

Ballouk explained that “in the live microscopy, [one] will find some changes consistent with [GN], 

there will be an infiltration and inflammation in the mesangial and the glomerular basement 

membrane . . . .” Tr. 197:2–5. In addition, Dr. Ballouk wrote “the lack of crescents on [Petitioner’s] 

biopsy does not mean that [Petitioner’s] vaccination did not aggravate her disease. [The b]iopsy 

is “the most proximate part of the renal tubule, extending from the glomerular capsule to the proximate 

straight tubule[.]” Tubulus Contortus Proximalis, DORLAND’S, https://www.dorlandsonline.com (last 

visited Feb. 3, 2021). The loop of Henle, or nephron loop, is “a long, U-shaped part of the renal tubule, 

extending through the medulla from the end of the proximal convoluted tubule to the beginning of the 

distal convoluted tubule.” The loop “begins with a descending limb having a thick-walled segment called 

the proximal straight tubule, followed by a thin-walled segment called the thin or attenuated tubule; this is 

followed by the ascending limb, which sometimes includes the distal end of the attenuated tubule and 

always ends with a long thick-walled segment called the distal straight tube.” Ansa Nephroni, 

DORLAND’S, https://www.dorlandsonline.com (last visited Feb. 3, 2021).

75 Prednisone is “a synthetic glucocorticoid derived from cortisone, administered orally as an 

antiinflammatory and immunosuppressant in a wide variety of disorders.” Prednisone, DORLAND’S, 

https://www.dorlandsonline.com (last visited Feb. 3, 2021).
25

was performed approximately [five] months post vaccination and [four] months after her first 

recorded elevated creatinine. Therefore, active disease could have ceased prior to biopsy.” Pet’r’s 

Ex. 50 at 2. When asked about the lack of crescents in Petitioner’s biopsy, Dr. Ballouk espoused 

that “[a]ctually, reviewing the literature about [crescents], [they don’t] exist [in] probably more 

than like [thirteen] percent [of patients] in this kind of [this] disease. So[,] this is not the disease 

where you will have crescents all the time.” Tr. 198:2–7. He also stated that “the timing also means 

[you] probably . . . will not see the crescents even if presented at – you know, so just to make it 

simple, you don’t have to see crescents to diagnose [FGN].” Tr. 198:9–12. When asked whether 

“the lack of crescents rule out . . . the probability that [Petitioner’s] vaccination may have 

accelerated her disease course[,]” Dr. Ballouk responded, “[n]o[,] . . . the literature say[s] that most 

of the time [doctors] will not see crescents at all.” Tr. 198:13–18. 

In his second expert report and corresponding testimony, Dr. Ballouk discussed “the 

manner in which [Petitioner’s] condition progressed differently as a result of vaccination than it 

would have otherwise.” Pet’r’s Ex. 50 at 1. He cited to and referenced multiple articles outlining 

the general FGN disease course. The first is an article by Nasr et al., which Dr. Ballouk described 

as “the largest, longest, single-center study of [FGN] patients . . . .” Pet’r’s Ex. 50 at 1; Resp’t’s 

Ex. A, Tab 5.76 The authors of this study wrote that the objective of the study was “[t]o better 

define the clinical-pathologic spectrum and prognosis [of FGN] . . . .” Resp’t’s Ex. A, Tab 5, at 1. 

The study included “[sixty-six] patients with FGN that were followed for a mean time of [fiftytwo] months.” Id. at 2. The sixty-six patients included sixty-three Caucasian patients, two Hispanic 

patients, and one Black patient, with a mean age of fifty-three at the time of biopsy. Id. at 2–3. At 

biopsy, seventy-one percent of patients had hypertension and fifty-nine percent had edema. Id. at 

4. All patients had proteinuria at the time of biopsy, with fifty-five percent of patients in the 

nephrotic range and thirty-eight percent of patients with full nephrotic syndrome. Id. at 3. The 

authors followed these patients for an average of 52.3 months, with a range of two to 209. Id. at 6. 

During this period, “[three] patients ([five percent]) had [complete remission], [five] patients 

([eight percent]) had [partial remission], [twenty-six] patients ([forty-three percent]) had 

[persistent renal disease], and [twenty-seven] patients (forty-four percent]) progressed to ESRD.” 

Id. The authors noted that “[g]ender, type of therapy, . . . presence of underlying malignancy, and 

presence of underlying autoimmune disease did not correlate significantly with outcome.” Id. The 

authors concluded that FGN “[p]rognosis is poor, with nearly one half of patients progressing to 

ESRD within [four] years.” Id. at 9. They also concluded that the clinical “[f]eatures associated

with poor renal outcome include older age, higher creatinine at biopsy, higher 24-hour urine 

protein at biopsy, and higher percentage of globally sclerotic77 glomeruli.” Id. 

Dr. Ballouk also discussed a paper by Javaugue et al. in which the authors conducted a 

retrospective study of “[twenty-seven] adults with [FGN] referred to [fifteen] nephrology 

departments in France between 1990 and 2011 . . . .” Tr. 201:19–202:19; Resp’t’s Ex. A, Tab 7, at 

1.78 Of these twenty-seven patients, there were sixteen men and eleven women, with a median age 

76 Samih H. Nasr et al., Fibrillary Glomerulonephritis: A Report of 66 Cases from a Single Institution, 6 

CLIN.J. AM. SOC. NEPHROL. 775 (2011).

77 Sclerotic means “hard, or hardening[.]” Sclerotic, DORLAND’S, https://www.dorlandsonline.com (last 

visited Feb. 2, 2021).

78 Vincent Javaugue et al., Long-term Kidney Disease Outcomes in Fibrillary Glomerulonephritis: A Case 

Series of 27 Patients, 62(4) AM.J. KIDNEY DIS. 679 (2016).
26

of fifty-nine. Resp’t’s Ex. A, Tab 7, at 2. The authors wrote that, “[a]t the time of diagnosis, most 

patients presented with hypertension ([seventy percent]) and lower-limb edema ([fifty-six 

percent]). All patients had proteinuria . . . with nephrotic syndrome in [eleven] patients ([forty-one 

percent] and microhematuria79 in [nineteen] patients ([seventy-three percent]).” Id. at 2–3. In terms 

of patient outcomes, the authors wrote that “[r]enal prognosis in [FGN] is poor and most prev iously 

reported patients progressed to ESRD.” Id. at 9 (citing id. at 10, Table 4). They continued, “[w]ith 

a median follow-up of [forty-six] months, [forty-eight percent] of patients from the present series 

developed ESRD after a median of [forty-four] months after diagnosis.” Id. at 9. 

During his testimony, Dr. Ballouk also stated that he relied on an article by Rosenstock et 

al. as a basis for his opinions. Tr. 202:20–203:1; Resp’t’s Ex. C, Tab 1; Resp’t’s Ex. A, Tab 8; 

Pet’r’s Ex. 23.

80 The authors of this article wrote that “[c]ontroversy surrounds the relatedness of 

. . . FGN and immunotactoid glomerulonephritis (“IT”)[,]” and they therefore set out “[t]o better 

define their clinicopathologic features and outcome[s by] . . . report[ing] the largest single center 

series of [sixty-seven] cases biopsied from 1980 to 2001, including [sixty-nine] FGN and [six] IT 

[cases].” Resp’t’s Ex. C, Tab 1, at 1. The FGN patients in this study included “[twenty-four] males 

and [thirty-seven] females . . . age [twenty-eight] to [eighty-one] years old . . . . These included 

[fifty-six] Caucasian, [three] African American, and [two] Hispanic patients.” Id. at 3. The authors 

also noted that, “at the time of biopsy,” forty-four of the sixty-one FGN patients had renal 

insufficiency, thirty-six of the patients had hypertension, and “[a]ll patients presented with 

proteinuria . . . .” Id. In terms of outcomes, the authors wrote that follow-up was conducted on 

fifty-six FGN patients. Id. at 6. These patients “were followed for a mean of [twenty-three] 

months[,]” and “[twenty-five] patients developed ESRD.” Id.The authors continued, “[w]hile only 

[eighteen percent] of patients who presented without renal insufficiency progressed to ESRD, 

[seventy-two percent] . . . of patients who presented with a creatinine [greater than] 2.0mg/dL 

reached ESRD.” Id. The authors found that “[t]he median time to ESRD was 24.4 [plus/minus] 

15.2 months (mean, 57.6 [months plus/minus] 9.49 months).” Id. The authors concluded that this 

study “confirm[s] the high risk of ESRD in FGN, with a median renal survival . . . of only [twentyfour] months from the time of biopsy.” Id. at 8. 

Based on these articles, Dr. Ballouk argued that Petitioner’s “[GN] advanced to ESRD 

much more rapidly than would be expected.” Pet’r’s Ex. 50 at 2. Dr. Ballouk opined that “[o]nly 

[forty-four] percent of . . . patients . . . will end up on dialysis with a median of [twenty -four] 

months.” Tr. 186:25–187:1. He relied on the Rosenstock et al. article to argue that Petitioner 

progressed to ESRD quicker than what is normally associated with an FGN patient. Tr. 204:21–

205:4. He stated:

If [one] look[s] at the literature, [one] would expect [Petitioner] to have – if she’s 

from the bad patients who end up on dialysis, . . . [they] usually [reach ESRD 

requiring dialysis in] two years . . . . [Petitioner] [reached ESRD requiring dialysis] 

79 Microhematuria, or microscopic hematuria, is “blood in the urine visible only with a microscope, 

defined as at least two to three red blood cells per high-power field.” Microscopic Hematuria, 

DORLAND’S, https://www.dorlandsonline.com (last visited Feb. 2, 2021).

80 Jordan L. Rosenstock et al., Fibrillary and Immunotactoid Glomerulonephritis: Distinct Entities with 

Different Clinical and Pathologic Features, 63 KIDNEY INTER. 1450 (2003).
27

in four months. So . . . [Petitioner progressed to ESRD requiring dialysis] at least a 

year and a half faster than the average.

Tr. 205:6–11. Regarding the Nasr et al. study, Dr. Ballouk wrote:

Applying the results of this study to [Petitioner’s] situation, . . . she advanced from 

biopsy to ESRD much more rapidly than expected. The average time from biopsy 

to ESRD was [fifty-two] months. [Petitioner], however, reached ESRD in only 

[four] months from the date of biopsy and only [seven] months from her first 

recorded elevated serum creatinine. This is a significant difference. 

Pet’r’s Ex. 50 at 2. Dr. Ballouk continued, “[w]hile it can be argued that [P]etitioner would likely 

have still reached ESRD at some point, she reached it much faster than the majority of other 

similarly situated [FGN] patients.” Id.

On cross-examination, Dr. Ballouk was asked about Petitioner’s onset date, which he 

argued was “seven to eight weeks before [her] symptomsstart[ed,]” or the “early part of September 

[2013].” Tr. 209:11–20. He explained that this estimation “has nothing to do with [Petitioner’s] 

vaccination[,]” but rather was based on “when [Petitioner’s] symptoms started, like the nausea, 

vomiting . . . .” Tr. 210:4–13. Dr. Ballouk agreed that kidney disease can be present without 

symptoms, but he stated that a person “may have some vague symptoms, but [the person] will not 

be aware” that she has a kidney disease. Tr. 210:14–211:1. Dr. Ballouk testified that Petitioner had 

“silent” kidney disease for “at least” a couple of months. Tr. 211:4–6. 

Dr. Ballouk also discussed Petitioner’s hypertension and edema on cross-examination. Dr. 

Ballouk agreed that hypertension was a clinical manifestation of kidney disease, but he stated that 

“hypertension is very, very common in overweight patients, so if [a person has] hypertension, it 

doesn’t mean [that person has a] kidney disease.” Tr. 211:12–17. However, after reviewing 

Petitioner’s medical records, Dr. Ballouk conceded that Petitioner had normal blood pressure 

readings in 2010 even though she was overweight and smoking at that time. Tr. 212:17–215:11. 

Dr. Ballouk also agreed that edema is a clinical manifestation of kidney disease. Tr. 216:2–5. He 

conceded that Petitioner’s primary care physician began documenting Petitioner’s edema 

approximately two years prior to her vaccination, although he again noted that “[o]bese patients 

like [Petitioner] . . . will have edema . . . but it doesn’t [mean] that [Petitioner] has kidney disease 

at that time . . . .” Tr. 216:8–15. However, Dr. Ballouk did acknowledge that Petitioner began 

having high blood pressure and edema findings at around the same time, in July 2011. Tr. 216:16–

217:2.

Rather, Dr. Ballouk asserted that Petitioner’s first clinical manifestation of her FGN 

occurred on November 21, 2013, when she presented to the hospital with complaints of abdominal 

pain, vomiting, nausea, and diarrhea. Tr. 217:7–218:1. Dr. Ballouk opined that these symptoms 

were all “clinical manifestations” of “renal insufficiency.” Tr. 218:5–9. However, upon 

questioning during cross-examination, Dr. Ballouk acknowledged that he did not refer to these 

symptoms as manifestations of renal insufficiency or kidney disease in his expert reports because 

he “indirectly [did as much when he] said that [Petitioner] had [GN] when she presented to the 

hospital. This is how [he] came to this conclusion, from [Petitioner’s] symptoms and labs.” Tr. 
28

218:10–18. Dr. Ballouk also conceded that he did not file any medical literature listing these 

symptoms as “clinical manifestations” of kidney disease, although he argued that “it’s well known 

that patients with renal insufficiency . . . will have nausea, . . . vomiting, . . . and sometimes . . . 

abdominal pain.” Tr. 218:19–219:1. When asked about the Clinical Practice Guidelines published 

by the National Kidney Foundation, which do not list these symptoms as manifestations of kidney 

disease or renal insufficiency, Dr. Ballouk responded that he “[did not] think [that] they mention 

every single manifestation, . . . but . . . any nephrologist will know that if [someone has] a rapid 

rise in BUN, [they] will feel bad and [they] may have nausea and vomiting.” Tr. 219:7 –15. Dr. 

Ballouk disagreed that these symptoms were likely a manifestation of a gastrointestinal illness 

(“GI”) because Petitioner had been complaining of these symptoms for two weeks, was also 

suffering from proteinuria, and had increased creatinine that did not improve with hydration. Tr. 

219:24–220:16. 

Dr. Ballouk also discussed Petitioner’s potential dehydration during her November 2013 

hospitalization and its effect on her creatinine levels. He testified that “it’s hard to say” exactly 

“how severe” her dehydration was. Tr. 229:7–8. However, he explained that “[t]he worse 

[Petitioner’s dehydration was,] the higher the creatinine [would be].” Tr. 229:13. When pressed, 

Dr. Ballouk stated that Petitioner was “moderately dehydrated[,]” and that her actual creatinine 

level, if she had not been dehydrated, would have been “around 1.5 to 1.7.” Tr. 229:15 –18, 21–

25. Dr. Ballouk explained that this estimation was based on his “personal experience[,]” although 

he later conceded that he did not cite to any medical literature as support. Tr. 230:3, 5–8. In 

addition, Dr. Ballouk stated that he would “expect to [see] some tachycardia81 and low blood 

pressure[]” in a person who is moderately dehydrated. Tr. 252:19–22. When asked whether 

Petitioner exhibited these symptoms during her hospitalization, Dr. Ballouk asserted that Petitioner 

had an initial normal pulse reading and high blood pressure when she presented to the hospital. Tr. 

250:24–252:4. Dr. Ballouk explained, however, that whether a person is exhibiting these 

symptoms “depends on the severity [of the dehydration] and it depends on the [patient’s] baseline 

[blood pressure and pulse levels].” Tr. 252:23–24. 

Under my questioning, Dr. Ballouk stated that vomiting and diarrhea are caused by renal 

failure when there is a “[rise] of the BUN and the creatinine . . . .” Tr. 256:2–8. He also explained 

that, “[o]n the other hand, . . . if you [are] vomiting and dehydrated, that will worsen your renal 

failure. It’s . . . a vicious cycle.” Tr. 256:17–19. When asked “how long it would take the effects 

of renal failure to lead to GI symptoms[]” in Petitioner’s case, Dr. Ballouk responded “a couple of 

months.” Tr. 256:24–257:4. 

Also, under my questioning, Dr. Ballouk estimated that Petitioner’s FGN began “around 

early September [2013].” Tr. 267:2–4. He agreed that the progression of Petitioner’s FGN up to 

the date of vaccination was “natural . . . because there [hadn’t] been any . . . catalyst to exacerbate 

her condition.” Tr. 268:7–10. However, he stated that Petitioner’s increase in creatinine between 

her November 2013 reading and January 2014 reading indicated that Petitioner’s disease was 

rapidly progressingduring that time. See Tr. 267:11–12. He clarified that he meant that Petitioner’s 

disease was “progressive [because of the rise in Petitioner’s creatinine and proteinuria between 

81 Tachycardia is “excessive rapidity in the action of the heart[.]” Tachycardia, DORLAND’S, 

https://www.dorlandsonline.com (last visited Feb. 2, 2021).
29

November and January], and it is aggressive because she ended up on dialysis [in] four months.” 

Tr. 280:12–281:1.

During re-direct examination, Dr. Ballouk opined that the presence of mesangial 

involvement, as well as the fact that Petitioner did not have one hundred percent sclerosed 

glomeruli, indicated that she was in the MES subgroup, which showed “exclusively mesangial 

proliferation or sclerosis” Tr. 274:20–275:1; Resp’t’s Ex. A, Tab 6, at 4. Citing the Rosenstock et 

al. study, Dr. Ballouk stated that a patient in the MES subgroup would take eighty months to reach 

ESRD. Tr. 275:2–5.

3. Respondent’s Expert, Dr. Levinson

Dr. Levinson submitted an expert report in which he wrote that he “disagree[s] with the 

claim that the [flu] vaccination accelerated the progression of [Petitioner’s] FGN to [ESRD].” 

Resp’t’s Ex. C at 3. He noted that while he “concur[s] with [Petitioner’s] diagnosis of FGN[,]” he 

“leave[s] detailed discussion of [the disease] to . . . [R]espondent’s expert in renal disease, and will 

focus on aspects of this disease that influenced formulation of [his] dissenting opinion.” Id. 

In his expert report, Dr. Levinson wrote that “[i]t is widely accepted that vaccines elicit the 

production of cytokines as a prerequisite for the induction of desired adaptive immune (antibody 

and cell-mediated) responses.” Id. at 5. He explained that the cytokine production “provides a 

favorable milieu in the lymph nodes that drain injection sites for promoting the activation of 

lymphocytes (B and T cells), which respond to the vaccine’s antigenic constituents.” Id. 

Therefore, Dr. Levinson wrote that the “production of cytokines, even proinflammatory cytokines, 

is an expected and desired outcome in vaccination strategy.” Id. 

However, Dr. Levinson further wrote that “[i]t is not immediately clear to [him]” what Dr. 

Gershwin was referring to when he wrote in his expert report that the “[flu] vaccine elicits a 

rigorous cytokine response . . . .” Id. (quoting Pet’r’s Ex. 19 at 3). Dr. Levinson opined that “it is 

highly unlikely that the cytokine response to the inactivated seasonal [flu] vaccine [received] by 

[Petitioner] reached a level of magnitude to deleteriously impact organs distant to the injection 

site.” Id. While Dr. Levinson wrote that the “[flu] virus . . . may induce intense lung inflammation 

and additional organ dysfunction due to the release of extremely large amounts of pro -

inflammatory cytokines,” a phenomenon he described as a “cytokine storm,” he explained that 

“there is no credible scientific evidence . . . that vaccines otherwise elicit such dangerous levels of 

cytokines.” Id. He testified that “[m]any of [the] people [who receive the flu vaccine] have 

underlying autoimmune diseases. Some of them are stable, some of them are not so stable.” Tr. 

119:11–13. He therefore concluded that “if Dr. Gershwin's . . . theory[] is correct, . . . [then] we 

would see a lot more reports of flu vaccine-induced exacerbations of autoimmune disease, and we 

just don't see that.” Tr. 120:12–19. 

Dr. Levinson wrote that “[t]he bottom line of the extant scientific literature is that 

inactivated vaccines, including seasonal [flu] vaccines, have not been shown to induce flares of 

disease activity in patients with stable autoimmune disease or augment disease expression in 

patients with active autoimmune disorders.” Id. Dr. Levinson testified that, while these studies do 

not directly address vaccination and FGN, he nonetheless explained that they are important 
30

because the Court “heard . . . from Dr. Gershwin that FGN may . . . represent an autoimmune 

disease, and to the extent that that may be true, then . . . what the studies that dealt with the effect 

of flu vaccine on autoimmune disease probably are relevant to FGN.” Tr. 115:25–116:11. He cited 

two articles as support. The first is by Westra et al. Resp’t’s Ex. C, Tab 2. 82 The authors of this 

article “provide an analysis of data on vaccination of patients with an [autoimmune inflammatory 

rheumatic diseases (“AIRD”)83].” Id. at 1. The authors note that “[s]afe vaccination is particularly 

important for patients with an AIRD, as vaccine-induced antigenic stimulation might exacerbate 

the underlying autoimmune disease.” Id. at 6. In terms of the flu vaccine specifically, the authors 

wrote that “several studies have found that autoantibody titers84 increase in some patients with an 

AIRD after [flu] vaccination,” although they note that “other studies could not confirm these 

findings, and in the majority of cases this increase . . . was not associated with clinical disease 

activity.” Id. Regarding RA, the authors noted that “[i]n most of the latest studies[,] . . . no 

significant influence of vaccination on disease activity has been reported.” Id. In addition, they 

noted that “in pre–post studies after [flu] vaccination, patients with RA did not experience 

increased disease activity.” Id. For patients with systemic lupus erythematosus (“SLE”),85 the 

authors wrote that “a number of studies” showed that “patients with SLE . . . did not develop more 

disease flares than unvaccinated patients with SLE.” Id. The authors did, however, further note 

that “[o]ther studies of patients with SLE found either no flares or mild flares . . . .” Id. They also 

noted that “[o]nly one severe disease manifestation[] (renal flares with [GN]) occurred in [one] of 

[twenty-nine] patients with SLE.” Id. at 6–7. However, the authors go on to note that “this study 

did not include a control of unvaccinated patients with SLE, and these data should therefore be 

interpreted with caution.” Id. at 7. The authors concluded that, “[i]n general, [flu] vaccination is 

safe for patients with SLE and inactive disease.” Id. The authors also found that “no increase in 

disease flares was found[]” in patients with granulomatosis with polyangiitis (“GPA”)86 when 

compared with non-vaccinated GPA patients. Id. Lastly, the authors wrote that “the inactivated 

[flu] vaccine seemed to be safe[]” after administration “[i]n a population of patients with diverse 

82 Johanna Westra et al., Vaccination of Patients with Autoimmune Inflammatory Rheumatic Diseases, 11 

NAT. REV. RHEUMATOL. 135 (2015). 

83 An autoimmune disease, generally, is “a disorder caused by an immune response directed against self 

antigens” that is typically characterized by “demonstrable circulating autoantibodies or cell-mediated 

immunity against autoantigen, inflammatory lesions caused by immunologically competent cells or 

immune complexes in tissues containing the autoantigens . . . .” Although autoimmune diseases generally 

involve evidence of pathogenic process, “some diseases, such as systemic lupus erythematosus and 

rheumatoid arthritis[,] are often classified as autoimmune diseases even though their pathogenesis is 

unclear.” Autoimmune Disease, DORLAND’S, https://www.dorlandsonline.com (last visited Feb. 2, 2021).

84 A titer is “the quantity of a substance required to produce a reaction with a given volume of another 

substance, or the amount of one substance required to correspond with a given amount of another 

substance. Titer, DORLAND’S, https://www.dorlandsonline.com (last visited Feb. 3, 2021).

85 Systemic lupus erythematosus is “a chronic, inflammatory, often febrile, multisystemic disorder of 

connective tissue that proceeds through remissions and relapses[]” that “is characterized principally by 

involvement of the skin . . . , joints, kidneys , and serosal membranes.” Systemic Lupus Erythematosus, 

DORLAND’S, https://www.dorlandsonline.com (last visited Feb. 2, 2021).

86 Granulomatosis with polyangiitis is “a multisystem disease chiefly affecting males, characterized by 

necrotizing granulomatous vasculitis involving the upper and lower respiratory tracts, glomerulonephritis, 

and variable degrees of the ANCA-associated type of small vessel vasculitis. Most authorities consider 

this condition to be an aberrant hypersensitivity reaction to an unknown antigen.” Granulomatosis with 

Polyangiitis, DORLAND’S, https://www.dorlandsonline.com (last visited Feb. 2, 2021).
31

AIRDs . . . .” Id. In addition, “[f]lares of SLE occurred as often after vaccination . . . in an 

unvaccinated control group . . . , and disease activity scores did not increase after vaccination.” Id.

The authors concluded that “[s]tudies comparing adverse effects between vaccinated and 

unvaccinated patients, and from pre–post vaccination studies, do not seem to indicate that 

vaccination exacerbates underlying AIRDs.” Id. at 8. They do note, “[h]owever, [that] serious 

vaccine-attributable conditions are rare; therefore, the clinical studies that have been done are too 

small to yield sufficient safety data.” Id.

The second article is by van Assen et al. Resp’t’s Ex. C, Tab 3.87 The authors of this article 

sought “to develop evidence-based European League Against Rheumatism (“EULAR”) 

recommendations for vaccination in patients with [AIRDs].” Id. at 1. The authors included 

“experts representing [eleven] European countries, consisting of eight rheumatologists, four 

clinical immunologists, one rheumatologist/clinical immunologist, one infectious disease 

physician, one nephrologist, one paediatrician[sic]/rheumatologist, and one clinical 

epidemiologist.” Id. They note that “[n]o studies have been performed comparing efficacy and 

harms between patients with AIRD with stable and unstable disease[]” and that “almost all 

vaccination studies in [AIRD] patients . . . addressed patients with quiescent disease.” Id. They 

further note that “[s]tudies that also included patients with moderate or severe disease activity did 

not show more frequent side effects or disease flares, or decreased efficacy in patients with [AIRD] 

compared with healthy controls.” Id. However, they nonetheless note that “the numbers of patients 

in these studies were too small to conclude that vaccination during active disease is safe and 

efficacious.” Id. Therefore, the authors recommended that “vaccination in patients with [AIRD] 

should ideally be administered during stable disease . . . .” Id. Regarding the inactivated flu 

vaccine, the authors wrote that “[a]dverse events of [flu] vaccination in patients with [AIRD] seem 

comparable to those in healthy controls, although there are no studies that are sufficiently powered 

with regard to safety.” Id. at 4. They recommend that “[i]nactivated [flu] vaccination should be 

strongly considered for patients with [AIRD].” Id. The authors conclude by writing that, 

“[a]lthough many case reports have been published demonstrating flares of AIRD or new-onset 

autoimmune diseases following vaccination, these adverse events remain rare and a causal 

relationship has not been proved.” Id. at 6. They continue, “several controlled studies show no 

difference in the occurrence of flares of AIRD after vaccination, although these studies have not 

been powered to address specific adverse events, but efficacy. Because of the lack of sufficiently

powered studies focusing on harms, these issues remain an important item on the research agenda.” 

Id. 

Dr. Levinson took issue with the studies that Dr. Gershwin cited “[t]o link the alleged 

vaccine-induced cytokines to [Petitioner’s] FGN,” which included “several studies that deal with 

1) the interaction of pro[-] and anti-inflammatory cytokines during the course of host immune 

responses . . . , and 2) the potential of pro-inflammatory cytokines to inflict renal tissue injury.” 

Resp’t’s Ex. C at 6 (citing Pet’r’s Exs. 24–42). Dr. Levinson wrote that the first group of studies 

“are of general interest and importance and have been appreciated for many years. However, they 

are not relevant to considerations in this case, as there is no credible evidence that any of the 

cytokines discussed are involved in the pathogenesis of FGN.” Id.In terms of the second group of 

studies, Dr. Levinson noted that, “although there is good evidence that pro-inflammatory cytokines 

87 S. van Assen et al., EULAR Recommendations for Vaccination in Adult Patients with Autoimmune 

Inflammatory Rheumatic Diseases, 70 ANN. RHEUM. DIS. 414 (2011). 
32

can cause renal tissue injury in other autoimmune diseases,” these studies concern “experimental 

animal models of autoimmune glomerulopathies and human autoimmune glomerulopathies in 

which tissue injury is initiated by antibodies that target renal tissue for destruction . . . .” Id.(citing 

Pet’r’s Exs. 27–31, 38, 40, 42). Dr. Levinson opined that he is “not aware of any credible evidence 

that such adaptive immune precipitants lead to the characteristic pathologic fibrillary changes seen 

in FGN and none of these factors were detected during the course of [Petitioner’s] diagnostic 

evaluation.” Id. He wrote that these articles “deal with studies in which renal tissue injury is 

attributed to pro-inflammatory cytokines that are produced locally, i.e., in the kidneys, by cells 

that are either renal tissue constituents or inflammatory cellular immigrants.” Id. (citing Pet’r’s 

Exs. 26–30, 38–42) (emphasis in original). Dr. Levinson contrasted that with Dr. Gershwin’s 

theory, which “proposed that cytokines produced at sites remote from the kidneys in response to 

the [flu] vaccine promoted damage to [Petitioner’s] kidneys.” Id. Dr. Levinson opined that “[t]here 

is no basis for such a claim unless [Dr. Gershwin] is invoking a vaccine-induced cytokine storm. 

And surely there is no evidence that this catastrophic event occurred.” Id. 

Regarding the onset of Petitioner’s FGN, Dr. Levinson wrote that “Dr. Gershwin is on 

shaky grounds when he makes claims about the vaccination aggravating a disease process whose 

time of onset relative to the vaccination is unclear to him.” Resp’t’s Ex. C at 4. Dr. Levinson took 

issue with Dr. Gershwin’s opinion that Petitioner’s “persistent nausea, emesis, diarrhea and 

abdominal pain . . . in the two weeks leading up to her [November 21, 2013] hospital visit were 

the by-products of an exacerbation of [her] FGN.” Id. Dr. Levinson described this conclusion as 

“a giant leap of faith[,]” and he instead opined that “those symptoms represented an unrelated

gastrointestinal illness.” Id. He continued that “it is extremely likely that this illness, which was

associated with intravascular volume depletion and resultant dehydration . . . contributed to the 

renal insufficiency that was first noted at that time.” Id. Dr. Levinson testified that Petitioner’s CT 

scan of her intestines showed “signs of acute diverticulitis.

88” Tr. 121:25–122:2. Dr. Levinson 

explained that “acute diverticulitis . . . is a pretty significant disorder[, which] . . . is associated

with inflammation . . . .” Tr. 122:3–6. In addition, Dr. Levinson discussed Petitioner’s blood tests 

conducted during her brief hospitalization, which showed “leukocytosis, [or] an elevated white 

cell count, which would go along with underlying inflammation, particularly an infection.” Tr. 

122:17–19. 

Dr. Levinson also took issue with Dr. Gershwin’s assertion that the flu vaccine 

exacerbated Petitioner’s FGN, resulting in Petitioner reaching ESRD faster than what is normally 

expected with this disease. Resp’t’s Ex. C at 4. In doing so, Dr. Levinson cited to the Rosenstock 

et al. article. See id.; see also Resp’t’s Ex. C, Tab 1.89 While Dr. Levinson agreed that “the median 

time of progression to [ESRD] in this . . . study . . . was reported to be 24.4 [plus/minus] 15.2 

months,” he noted that, “clearly, the length of progression time is influenced by the pathology seen 

on renal biopsy.” Resp’t’s Ex. C at 4. In the article, the authors wrote that, of the sixty-one patients

88 Diverticulitis is “inflammation of a diverticulum, especially inflammation related to colonic diverticula, 

which may undergo perforation with abscess formation.” Diverticulitis, DORLAND’S, 

https://www.dorlandsonline.com (last visited Feb. 2, 2021). The diverticulum is “a circumscribed pouch 

or sac of variable size occurring normally or created by herniation of the lining mucous membrane 

through a defect in the muscular coat of a tubular organ. Diverticulum, DORLAND’S, 

https://www.dorlandsonline.com (last visited Feb. 2, 2021).

89 Rosenstock et al., supra note 80.
33

with FGN included, forty-four percent of biopsies showed MPGN defined by mesangial expansion 

with foci of mesangial interposition and replication of glomerular basement membrane90 . . . .” 

Resp’t’s Ex. C, Tab 1, at 4. In addition, “[t]wenty-one percent of biopsies had exclusively 

mesangial proliferation or sclerosis (“MES”)[,]” while “[f]ifteen percent of patients had a diffuse 

proliferative (“DPGN”)

91 pattern characterized by endocapillary proliferation including focal 

infiltrating leukocytes . . . .” Id. The authors further noted that seven percent of biopsies revealed 

a “membranous [pattern],92 featuring predominantly subepithelial93 fibrillar deposits separated by 

well-formed basement membrane spikes, with little or no mesangial hypercellularity[,]94” and 

another “[t]hirteen percent of biopsies had a nondescript diffuse95 sclerosing96 pattern (“DS”), 

defined as glomerular sclerosis97 obliterating [greater than seventy percent] of glomeruli . . . .” Id.

While the authors did note that “[t]he median time to ESRD was 24.4 [plus/minus] 15.2 months[, 

with a] mean [of] 57.6 [plus/minus] 9.49 months[,]” they explained further that the “[m]ean time 

to ESRD varied according to histologic subgroups.” Id. at 6. They wrote that “[t]he histologic 

subgroups of DS, DPGN, and MPGN progressed more rapidly to ESRD[, with a] mean [of seven] 

. . . , [twenty] . . . , and [forty-four] months[] respectively[,] compared to MES and MGN 

[subgroups, with a] mean [of eighty] . . . and [eighty-seven] months[] respectively[].” Id. 

Based on this study, Dr. Levinson wrote that “patients with the chronic irreversible change 

of [DS] demonstrated a shorter time of progression from the time of diagnosis to [ESRD], 

compared to patients with other histopathological subtypes.” Resp’t’s Ex. C at 4. He further noted 

that Petitioner’s “renal biopsy demonstrated extensive histopathological signs of chronic and 

irreversible disease including [DS]. Therefore, her rate of progression to [ESRD] would be 

expected to be commensurate with the time period reported for such FGN patients studied in” the 

Rosenstock et al. article. Id. Dr. Levinson wrote that Petitioner exhibited “[i]mpaired renal function 

(creatinine of 2.8), proteinuria and hematuria . . . when she presented to [MVH] on November 21, 

90 Glomerular membrane refers to “the fenestrated basement membrane of the visceral layer of the 

glomerular capsule, lying adjacent to glomerular capillaries . . . .” Glomerular Membrane, DORLAND’S, 

https://www.dorlandsonline.com (last visited Feb. 2, 2021).

91 Diffuse glomerulonephritis is “a severe form in which there are proliferative changes in more than half 

the glomeruli, frequently with epithelial crescent formation and necrosis[. I]t is often seen in cases of 

advanced [SLE].” Diffuse Glomerulonephritis, DORLAND’S, https://www.dorlandsonline.com (last visited 

Feb. 2, 2021).

92 This refers to membranous glomerulonephritis, which is “glomerulonephritis characterized 

histologically by proteinaceous deposits on the glomerular basement membrane or by thickening of the 

membrane, with circulating antigen-antibody complexes, indicating immune complex disease.” 

Membranous Glomerulonephritis, DORLAND’S, https://www.dorlandsonline.com (last visited Feb. 3, 

2021).

93 Subepithelial means “beneath the epithelium.” Subepithelial, DORLAND’S, 

https://www.dorlandsonline.com (last visited Feb. 3, 2021).

94 Hypercellularity is “a state characterized by an abnormal increase in the number of cells present . . . .” 

Hypercellularity, DORLAND’S, https://www.dorlandsonline.com (last visited Feb. 3, 2021).

95 Diffuse means “not definitely limited or localized; widely distributed.” Diffuse, DORLAND’S, 

https://www.dorlandsonline.com (last visited Feb. 3, 2021).

96 Sclerosing is “causing or undergoing sclerosis.” Sclerosing, DORLAND’S, 

https://www.dorlandsonline.com (last visited Feb. 3, 2021).

97 Glomerular sclerosis, or glomerulosclerosis, is “fibrosis and scarring with senescence of the renal 

glomeruli.” Glomerularsclerosis, DORLAND’S, https://www.dorlandsonline.com (last visited Feb. 3, 2021).
34

2013.” Id. He explained that Petitioner began “[PD] . . . in June[] 2013 [sic].

98” Id. Therefore, he 

calculated that “the approximate time of her progression to [ESRD] from the time of her diagnosis 

of a glomerulopathy was seven months and is totally consistent with the time period observed in” 

the Rosenstock et al. article. Id. 

During cross-examination, Dr. Levinson opined that the time period measured in the 

Rosenstock et al. article “was . . . the time of diagnosis to the time of entering [ESRD].” Tr. 151:23–

152:3. After further questioning, Dr. Levinson conceded that “it’s not particularly clear[]” whether 

this article was measuring from the time of diagnosis to ESRD or the time of biopsy to ESRD. Tr. 

153:5–10. Dr. Levinson explained “that based on the reading [he] did, . . . [he] assumed that that 

was from the time of diagnosis with a clinical disease of nephritis.” Tr. 154:24–155:2. 

4. Respondent’s Expert, Dr. Fine

Dr. Fine wrote that FGN “is a poorly understood entity with limited treatment options.” 

Resp’t’s Ex. A at 7. While he acknowledged that the causes of FGN are “unknown,” Dr. Fine 

explained that FGN “has been associated with hematologic and nonhematologic malignancies, 

plasma cell dyscrasias,

99 autoimmune disease and [H]epatitis C.” Id. Dr. Fine found it “notable 

that [FGN] has never been associated with the [flu] vaccine or any other vaccine.” Id. He then 

discussed an association between FGN and Oxycodone use. See id. However, during his testimony, 

Dr. Fine clarified that he did not believe that Petitioner’s Oxycodone use caused her FGN. Tr. 

300:22–24. He explained that he included this discussion in his expert reports “because if someone 

is going to claim that a flu vaccine did it and there's never been a publication and she's on a 

substance that has been described as causing . . . [FGN], then at least there's a paper on something 

else that she is exposed to.” Tr. 301:1–6. He continued, “[s]o if one is going to speculate that a

vaccine did it and there's no data and you've got something that she is taking and there is data, it 

makes [Oxycodone use] more likely than at least the flu shot.” Tr. 301:6–9. Dr. Fine concluded 

this discussion by stating that, “as of now, [he does not] have any reason to believe that Oxycodone 

was certainly not more likely than not [the cause of Petitioner’s FGN].” Tr. 301:13–14. In fact, Dr. 

Fine believed that it was “much less likely than not that Oxycodone was the culprit.” Tr. 301:15–

16.

Regarding Petitioner’s health pre-vaccination, Dr. Fine opined that she exhibited two 

symptoms that are considered manifestations of kidney disease. The first is hypertension. Resp’t’s 

Ex. A at 4–5. Dr. Fine wrote that “[h]ypertension is a well[-]described feature of chronic kidney 

disease.” Id. at 5. He cited to the National Kidney Foundation’s Clinical Practice Guidelines for 

98 Petitioner had her PD catheter placed in June 2014, which would be seven months from November 

2013. See Pet’r’s Ex. 4 at 2–3. It is clear based on context that Dr. Levinson’s reference to June 2013 is a 

typographical error.

99 Plasma cell dyscrasias are “a diverse group of neoplastic diseases involving proliferation of a single 

clone of cells producing a serum M component (a monoclonal immunoglobulin or immunoglobulin 

fragment).” Plasma Cell Dyscrasias, DORLAND’S, https://www.dorlandsonline.com (last visited Feb. 3, 

2021). An M component is “an abnormal monoclonal immunoglobulin with a characteristic 

electrophoretic pattern, occurring in the serum of patients with plasma cell dyscrasias and formed by the 

proliferating concentrations of immunoglobulin-producing cells.” M Component, DORLAND’S, 

https://www.dorlandsonline.com (last visited Feb. 3, 2021).
35

Chronic Kidney Disease: Evaluation, Classification and Stratification as support. Id.; Resp’t’s Ex. 

A, Tab 1.100 The guidelines state that “[h]igh blood pressure is both a cause and a complication of 

chronic kidney disease.” Resp’t’s Ex. A, Tab 1, at 45. When hypertension arises “[a]s a 

complication, [it] may develop early during the course of chronic kidney disease and is associated 

with adverse outcomes – in particular, faster loss of kidney function and development of 

cardiovascular disease.” Id. Dr. Fine also cited to an article by Coresh et al. as support. Resp’t’s 

Ex. A at 5; Resp’t’s Ex. A, Tab 3.101 In this study, the authors conducted “[a] cross-sectional study 

of a representative sample of the US population . . . using 16,589 adult participants aged 

[seventeen] years and older . . . .” Resp’t’s Ex. A, Tab 3, at 1. They defined elevated serum 

creatinine as 141 μmol/L or higher (~1.6 mg/dL) for men and 124 μmol/L or higher (~1.4 mg/dL) 

for women (>99th percentile for healthy young adults) . . . .” Id. The authors found that, among 

others, “[h]igher systolic and diastolic blood pressures, presence of hypertension, [and] 

antihypertensive medication use . . . were all associated with higher serum creatinine levels.” Id. 

They further noted that “[a]n estimated [three percent] (5.6 million) of the civilian, 

noninstitutionalized US population had elevated serum creatinine levels, [seventy percent] of 

whom were hypertensive.” Id.

Furthermore, Dr. Fine testified that he submitted two additional articles “that document[] 

the prevalence of hypertension in patients with FGN[,]” which show that “around [seventy]

percent” of FGN patients have hypertension. Tr. 194:2–12. The first of these articles is by Nasr et 

al., which was also discussed by Dr. Ballouk and described in more detail in section III.B.2 above. 

The authors of this article wrote that, of the sixty-six FGN patients studied, seventy-one percent 

presented with hypertension. Resp’t’s Ex. A, Tab 5, at 1. The second article, by Javaugue et al., 

was also discussed by Dr. Ballouk and described in section III.B.2 above. Resp’t’s Ex. A, Tab 7. 

The authors of this article wrote that, “at the time of diagnosis,” seventy percent of the patients 

they studied “presented with hypertension . . . .” Id. at 2. 

Dr. Fine stated these four studies are relevant because “when [hypertension] appears when 

you're not expecting it, it suggests the possibility of kidney disease . . . .” Tr. 294:19–21. He 

explained that “hypertension . . . is often the first sign of kidney disease,” and that “in the presence 

of [CKD], whatever [the] cause, hypertension is very frequent, maybe even [occurring] the 

majority of the time as . . . one’s disease progresses.” Tr. 294:23–295:11. He further explained that 

“in the context of what happened to [Petitioner], it makes sense that [hypertension] was the onset 

of her kidney disease.” Tr. 294:21–22. Regarding Petitioner, Dr. Fine explained that “her blood 

pressure measurements from August 2010 to May 2011 were very stable and ranged from 112–

122/62–80 . . . . This appears to be her stable baseline blood pressure.” Resp’t’s Ex. A at 2. He 

noted that Petitioner’s “blood pressure [was] first noted to be elevated in July and August of 2011, 

long before her vaccine exposure.” Id. at 4. Dr. Fine stated that Petitioner’s heart rate was also 

higher than her baseline when she had her initial high blood pressure readings. Id. Dr. Fine 

acknowledged that her higher heart rate on these initial occasions might indicate that her high 

blood pressure readings were due to pain or anxiety. Id. at 2–3. He noted, however, that she had 

blood pressure and heart rate readings within her baseline range in May 2011, when she also had 

100 National Kidney Foundation, K/DOQI Clinical Practice Guidelines for Chronic Kidney Disease: 

Evaluation, Classification and Stratification, 39 (Supp. 1) AM.J.KIDNEY DIS. S1 (2002). 

101 Josef Coresh et al., Prevalence of High Blood Pressure and Elevated Serum Creatinine Level in the 

United States, 161 ARCH. INTERN. MED. 1207 (2001).
36

a pain score of 7/10. Id. at 3. Regarding Petitioner’s blood pressure readings, Dr. Fine continued, 

“[a]fter [July and August 2011], while they intermittently returned to baseline levels, [Petitioner’s] 

blood pressures were generally higher than the prior baseline, fluctuated more[,] and were 

interspersed with spikes in blood pressure . . . .” Id. at 4–5. Dr. Fine also noted that, “[m]ost 

importantly, [Petitioner’s] highest blood pressure of 176/124 . . . occurred on August 20, 2013, 

approximately a month prior to administration of the influenza vaccine on September 23, 2013 . . 

. .” Id. at 5. Dr. Fine concluded that “[t]hese blood pressure changes suggest that [Petitioner’s] 

kidney disease was present for some time prior to diagnosis, and the very severe elevation in 

August 2013[,] certainly suggests that the disease was already flaring prior to the September 2013 

vaccination.” Id. 

In addition to hypertension, Dr. Fine also stated that Petitioner’s “lower extremity edema,” 

noted on at least three separate visits prior to her vaccination, were manifestations of her FGN. Tr. 

298:14–20. Dr. Fine noted that “edema is quite common[]” in kidney disease patients. Tr. 298:24–

299:1. He explained that edema is “really a reflex of the ability of the kidney to get rid of fluid, 

although ultimately it’s more related to salt than fluid. . . . [T]he two go hand[-]in[-]hand.” Tr. 

299:1–4. He further explained that:

if you have either a declining kidney function, you could get fluid, or if you have 

excessive wasting of protein in the urine, people tend to retain sodium and get 

swollen as well. It's not specific for kidney disease, but in someone who has no 

other explanation, one has to consider kidney disease as being one of the

possibilities.

Tr. 299:5–11. In the Javaugue et al. study discussed above, the authors wrote that fifty-six percent 

of the patients studied had “lower-limb edema” at the time of FGN diagnosis. Resp’t’s Ex. A, Tab 

7, at 2. 

Dr. Fine, however, stated that he did not believe that the Petitioner’s symptoms of 

abdominal pain, nausea, vomiting, and diarrhea when she presented to the hospital on November 

21, 2013, were the manifestation of her FGN. Tr. 302:24–303:8. He explained that “kidney disease

does not usually present with these symptoms.” Tr. 303:10–11. While he noted that “nausea and 

vomiting are well established symptoms of advanced kidney disease[,]” Dr. Fine explained that 

they are “just generally not symptoms [he’s] going to see until . . . [a] very advanced [glomerular 

filtration rate (“GFR”)102 . . . .” Tr. 303:11–12, 17–18. Dr. Fine also stated that “[d]iarrhea is not a 

symptom of kidney disease that he’s ever heard of.” Tr. 303:20–21. Dr. Fine noted that “patients 

with kidney disease [may] present with diarrhea for some other reason[,]” but stated that, “in 

general, as a manifestation of either acute or [CKD], diarrhea is not something that would make 

[him] think . . . [someone has a] kidney disease.” Tr. 303:24–304:2. Rather, Dr. Fine opined that 

102 The glomerular filtration rate is “the quantity of glomerular filtrate formed per unit time in all 

nephrons of both kidneys, equal to the inulin clearance; usually measured clinically by the endogenous 

creatinine clearance.” Glomerular Filtration Rate, DORLAND’S, https://www.dorlandsonline.com (last 

visited Feb. 3, 2021). Glomerular filtrate is “the ultrafiltrate of plasma that passes across the membranes 

of the renal corpuscles into the urinary space.” Glomerular Filtrate, DORLAND’S, 

https://www.dorlandsonline.com (last visited Feb. 3, 2021).
37

Petitioner’s symptoms would have “immediately [put] the focus . . . on abdominal issues.” Tr. 

304:5–7. 

In addition, Dr. Fine argued that three diagnostic findings show that Petitioner likely was 

suffering from a gastrointestinal illness at the time of her November 21,2013hospitalization. First, 

Dr. Fine noted that Petitioner had “a high white blood cell count” during her brief hospitalization. 

Tr. 304:7–8. He further stated that “Dr. Ballouk made an allusion to [Petitioner’s] volume 

depletion, . . . the idea [being] as you lose water in the blood, the white [cell] count concentration 

goes up. That is not an accepted teaching. Hemoglobins103 can go up when you get volume 

depleted, white [cell] counts generally don’t.” Tr. 306:11–15. Dr. Fine explained that “white cell 

counts don’t go up just because of kidney failure. Generally[,] a high white blood cell count 

suggests an inflammatory or an infectious condition.” Tr. 306:8–10. Furthermore, Dr. Fine 

explained that “if the white count went up because of hemodilution,104 all the subtypes of white 

cells would go up together, but in her case, the one that indicates infection was actually higher than 

all the rest.” Tr. 306:1–19. Therefore, he concluded “that the higher white cell count was not a 

feature of volume depletion[] but was truly a high white blood cell count.” Tr. 306:21–23. 

Second, Dr. Fine stated that, “on [Petitioner’s] white count, there was what [is] . . . call[ed] 

a left shift.” Tr. 304:13–14. He explained a “left shift” is “a high number of neutrophils,105 which 

generally suggests an infection.” Tr. 304:14–15. Third, Dr. Fine noted that Petitioner’s abdominal 

“CT did show something that suggested a mild diverticulitis.” Tr. 304:18–19. He explained that 

diverticulitis “is little appendices on the other side of the bowel.” Tr. 305:2–3. He disagreed with 

Dr. Ballouk that diverticulitis cannot last “for [only] two weeks,” as “there are cases of 

diverticulitis that spontaneously resolve.” Tr. 304:20–23. In addition, Dr. Fine testified that “[t]he 

other feature that suggests . . . that this was gastrointestinal is [that] it resolved, and . . . [Petitioner] 

specifically [stated] that after this, she had intolerance of milk products . . . .” Tr. 305:3 –8. He 

explained that “one of the most common causes of [lactose intolerance] is a gastroenteritis106 type 

of presentation.” Tr. 305:15–16. Dr. Fine opined that, taken together, “it’s sort of added evidence 

that this was just a GI complaint.” Tr. 306:20–21.

Dr. Fine also discussed the renal function testing performed during Petitioner’s brief 

hospitalization and her estimated GFR (“EGFR”). In terms of testing renal function, Dr. Fine 

explained that “the standard test that [doctors] use, the most . . . reliable test [doctors] have is the 

creatinine [test].” Tr. 307:5–6. Dr. Fine further explained that creatinine levels differ person to 

person, where “creatinine in a very muscular person tends to be higher because it's made by [the] 

103 Hemoglobin is “the red oxygen-carrying pigment of the erythrocytes, formed by developing 

erythrocytes in bone marrow.” Hemoglobin, DORLAND’S, https://www.dorlandsonline.com (last visited 

Feb. 4, 2021). 

104 Hemodilution is an “increase of the fluid content of the blood with resulting decrease in concentration 

of its erythrocytes.” Hemodilution, DORLAND’S, https://www.dorlandsonline.com (last visited Feb. 4, 

2021).

105 Neutrophils are “mature granular leukocytes that [are] polymorphonuclear (its nucleus having three to 

five lobes connected by slender threads of chromatin, and cytoplasm containing fine granules).” 

Neutrophil, DORLAND’S, https://www.dorlandsonline.com (last visited Feb. 3, 2021).

106 Gastroenteritis is “inflammation of the lining of the stomach and intestines . . . .” Gastroenteritis, 

DORLAND’S, https://www.dorlandsonline.com (last visited Feb. 4, 2021).
38

muscle[s], and in someone who is less muscular, it will be lower.” Tr. 307:22–25. Because “age, 

race and gender all affect muscle mass indirectly[,]” Dr. Fine testified that there is a “calculation, 

or . . . formula that’s used[]” to “measure . . . the ability of the kidney to clear toxins.” Tr. 307:25–

308:2, 9–10. Dr. Fine explained that the formula “includes the creatinine [level], but then it tries 

to normalize that to the other features by looking at age, race[,] and gender[,]” and the number 

calculated by this formula is called the GFR. Tr. 308:2–8. He noted that “[t]he lower your GFR, 

the less well you clear toxins.” Tr. 308:10–11. Dr. Fine testified that a “normal” GFR is “more 

than [ninety].” Tr. 308:17. He further testified that the GFR “more or less reflects percent of kidney 

function. So[,] if [GFR is] at [twenty], [then that person] has [twenty] percent of the normal kidney 

function.” Tr. 308:18–20. 

Dr. Fine explained that there are five stages of kidney disease and that “the staging of 

kidney disease is specifically based on [EGFR].” Tr. 308:23–309:1. Dr. Fine testified that the 

stages of kidney disease are as follows:

Stage one is when the EGFR is more than [ninety]; stage two is [sixty] to [eightynine]; stage three [is thirty] to [fifty-nine]; and then stage four is [fifteen] to [thirty]

. . . Stage five is less than [fifteen] and that's usually considered sort of near [ESRD], 

or [ESRD].

Tr. 309:1–6.107 Dr. Fine explained that an EGFR of “below [fifteen is] . . . when [doctors] really 

start to monitor patients very closely for dialysis needs[,]” which usually begins once the patient 

exhibits “symptoms like nausea and vomiting, poor appetite.” Tr. 309:6–9. 

During Petitioner’s November 21, 2013 hospitalization, Dr. Fine noted that her creatinine 

level was 2.8, which equated to an EGFR of “20 ml/min/1.73m2[,] representing approximately 

[twenty percent] of kidney function.” Resp’t’s Ex. E at 3–4. Dr. Fine testified that this meant that 

Petitioner was already in stage four of her kidney disease by her November 21, 2013 

hospitalization. Tr. 309:10–14. Dr. Fine disagreed with Dr. Ballouk’s contention that Petitioner’s 

creatinine was as high as it was because she was dehydrated. Tr. 309:15–19. While he agreed that 

“if [Petitioner] had gotten fluids and [doctors] rechecked her creatinine, it would probably have 

been a little lower[,]” Dr. Fine opined that he did not “think that it would be less than two . . . .” 

Tr. 309:19–22. He estimated that Petitioner’s creatinine after receiving fluids was “probably 

somewhere around 2.5, but certainly it wouldn't have been a dramatic reduction in her creatinine 

and hence [not a drastic] increase in that GFR number . . . . [Y]ou can have a creatinine of 2.4, 2.5, 

[and] her GFR is still in the low [twenties].” Tr. 310:9–14. Further, Dr. Fine addressed the 

difference between Petitioner’s creatinine readings in November 2013 and January 2014. He 

explained that, as kidney function worsens, “the creatinine rises way faster than the amount of 

kidney function you lose.” Tr. 311:11–15. He continued that this did not result in a “massive 

change” in Petitioner’s EGFR. Tr.311:19–12. Dr. Fine stated that the rise in Petitioner’s creatinine 

107 Dr. Fine’s testimony on the stages of kidney disease by EGFR closely tracks with the Kidney Disease 

Improving Global Outcomes’ 2012 Clinical Practice Guidelines for the Evaluation and Management of 

Chronic Kidney Disease that Dr. Fine submitted with his supplemental report. See Resp’t’s Ex. E, Tab 4, 

at 21; Kidney Disease Improving Global Outcomes, 2012 Clinical Practice Guidelines for the Evaluation 

and Management of Chronic Kidney Disease, 3(1) KIDNEY INTERN. SUPP. 1, 21 (2013). 
39

levels did not signal rapid progression because “[r]apidly progressive patients lose . . . half their 

kidney function in weeks.” Tr. 311:22–24.

Dr. Fine took issue with how Petitioner characterized the Nasr et al. study and applied it to 

her disease progression. He testified that this study was “a case series, which is just a number of 

patients . . . [where researchers] look at what happens to [the patients] and how they presented . . 

. .” Tr. 313:11–13. He wrote that this “study is a retrospective one which is not designed to predict 

‘expected’ progression.” Resp’t’s Ex. E at 3. Rather, Dr. Fine opined that “[i]t is a descriptive 

study that presents a series of patients and how their disease behaved in order to give the reader

insights into the disease.” Id. 

Nevertheless, Dr. Fine explained that “the features of [Petitioner’s] disease, both clinical 

and histopathologic, are entirely consistent with those presented in this study of a relatively small 

patient population with a rare disease.” Id. Specifically, Dr. Fine referred to a chart on page seven 

of the article, which “shows . . . the four factors that would predict, in their group of patients, at 

the time of biopsy, which [patient] is going to do the worst.” Tr. 314:14–19. In the article, the 

authors “identifiedseveral independent predictors of ESRD by multivariate analysis. . . .” Resp’t’s 

Ex. A, Tab 5, at 9. They listed “older age, higher creatinine at biopsy, higher 24-hour urine protein 

at biopsy, and higher percentage of globally sclerotic glomeruli” as “predictors of renal survival 

in [FGN].” Id. Dr. Fine explained each predictor in greater detail during his testimony. He 

explained that, for the old age factor, “the older you are, your hazard ratio is one more, for each 

year in age, you have 0.12 percent, or [twelve] percent increased risk [of reaching ESRD].” Tr. 

314:21–23. For the urine protein factor, Dr. Fine stated that “the higher the urine protein, the more 

likely [the patient is] going to be on dialysis.” Tr. 314:25–315:2. Regarding serum creatinine at 

biopsy, Dr. Fine explained that “the higher that is, the greater risk of meeting [ESRD, which] . . . 

make[s] sense[] because . . . if you have higher creatinine, [then] you have more damage to your 

kidneys and are more likely to end up on dialysis.” Tr. 315:3–8. Lastly, he explained that “globally 

sclerotic glomerulus is a dead glomerulus, [and] the more you have, the more likely you’re going 

to be on dialysis.” Tr. 315:9–12.

Looking at these factors, Dr. Fine opined that Petitioner “had high levels of proteinuria and 

creatinine at [the] time of biopsy and very high percent of sclerosed glomeruli.” Resp’t’s Ex. A at 

7. The only factor Dr. Fine did not believe applied to Petitioner was age. Tr. 316:2–3. Therefore, 

Dr. Fine concluded that “[i]t is not surprising . . . that she went on to develop ESRD.” Resp’t’s Ex. 

A at 7. 

Dr. Fine also discussed Petitioner’s renal biopsy results in detail in both his written reports 

and testimony. Dr. Fine testified that he believed that “there are significant clues as to how long 

[Petitioner’s FGN] was there based on [her] biopsy [results].” Tr. 312:12–14. He discussed three 

articles as support. The first was the Nasr et al. article. In this article, which studied sixty-six FGN 

patients, the authors noted that only one of the patients had a form of FGN called “diffuse 

sclerosing glomerulonephritis” (“DSGN”), which they defined as “[one hundred percent] of 

glomeruli showing global sclerosis.” Resp’t’s Ex. A, Tab 5, at 3–4. They also noted that “fiftyfive cases ([eighty-three percent]) showed interstitial inflammation, which was predominantly 

focal.” Id. at 4. In addition, they found that “[t]he degree of tubular atrophy and interstitial fibrosis 

ranged from absent ([six percent] of cases) to mild ([fifty-one percent]) to moderate ([thirty-three 
40

percent]) to severe ([nine percent]).” Id. The authors also found that the “[m]ean percentage of 

globally sclerotic glomeruli” was twenty-five percent. Id. at 5. 

In addition to the Nasr et al. study, Dr. Fine also referenced the Rosenstock et al. study in 

support of his discussion of Petitioner’s biopsy results. Dr. Fine testified that this study “actually 

break[s FGN] down . . . based on pathology findings . . . .” Tr. 318:22–319:2. The authors of this 

study wrote that “[t]hirteen percent of biopsies had a nondescript diffuse sclerosing pattern . . . , 

defined as glomerular sclerosis obliterating [greater than seventy percent] of glomeruli . . . .” 

Resp’t’s Ex. C, Tab 1, at 4. They also wrote that “[i]nterstitial disease was most severe in the 

[diffuse sclerosing] subgroup, in which all biopsies . . . displayed moderate to severe interstitial 

fibrosis . . . .” Id. While the authors found that “[t]he [overall] median time to ESRD was 24.4 

[plus/minus] 15.2 months,” with an overall “mean [time to ESRD] of 57.6 [plus/minus] 9.49 

months[,]” they further noted that the “[m]ean time to ESRD varied according to histologic subtype 

. . . .” Id. at 6. They found that the diffuse sclerosing “subgroup[] . . . progressed more rapidly to 

ESRD” than other subgroups, noting that patients of this group reached ESRD in a mean of seven 

months. Id. A chart created by the authors showed that more than seventy percent of the diffuse 

sclerosing subgroup of patients reached ESRD within two months from the date of biopsy. Id. at 

10. 

During his testimony, Dr. Fine also discussed the Rosenstock and Markowitz article, which 

he described as a “more of a review type paper.” Tr. 326:16–17; Pet’r’s Ex. 55. On page two of 

this article, the authors provide a chart in which they list the clinical characteristics of patients with 

FGN included in the three studies reviewed by the authors. Pet’r’s Ex. 55 at 2. The authors found 

that, “[a]t the time of presentation, [seventy percent] of patients had renal insufficiency, and the 

mean serum creatinine was 2.9 . . . .” Id. at 1. They further noted that “[t]he mean [twenty-four]-

hour urine protein was 5.7 . . . , and [thirty-six percent] of patients met criteria for full nephrotic 

syndrome.” Id. Dr. Fine stated that this study demonstrates that Petitioner’s FGN was a “classic” 

presentation. Tr. 327:20.

Regarding Petitioner’s renal biopsy, Dr. Fine wrote that the “biopsy findings are typical of 

an advanced [FGN] as described in the literature.” Resp’t’s Ex. A at 5. He noted that the biopsy 

revealed “extensive interstitial inflammation.” Tr. 340:23–24. He further noted that “[eighteen] 

out of [twenty-three] of [Petitioner’s glomeruli] . . . were dead glomeruli[,]” and “three other

glomeruli that show segmental sclerosis, so it's starting to scar off, but it's probably an earlier stage 

scarring, with a significant lesion, glomerular tufts, and [the pathologists] say, ‘glomeruli show 

marginal increase in mesangial matrix . . . .” Tr. 339:10–12, 342:2–7. The results also revealed a 

“mild increase in cellularity due to few mononuclear cells. So[,] the few mononuclear cells say

[there’s] maybe a little bit of inflammation, but this mesangial matrix increases the mesangial type 

lesion.” Tr. 342:9–12. He continued, “in the three glomeruli that [he] ha[s] that [he] can actually 

get real information out of, there isn't any evidence of something that's highly active.” Tr. 342:12–

15. He further testified that the pathologists wrote “[t]he glomeruli do not show evidence of

crescent formation, fibrinoid necrosis, thrombosis, or endocapillary proliferation.” Tr. 343:2–4. 

Dr. Fine opined that they wrote this “because they want [the nephrologist reading the results] to

know that, because it's actually important in determining how active is the lesion.” Tr. 343:5–8. 

Dr. Fine argued that Petitioner’s theory that she “had a rapid loss of kidney function” fails because 

that type of deterioration doesn’t happen “without crescentic GN or some really aggressive 
41

inflammation[,] which almost always results in crescentic formation.” Tr. 344:9, 16–18. Dr. Fine 

opined that “[i]f there was ongoing active disease that was bad enough to cause renal failure from 

September through to the time of the biopsy,” then “you would see evidence of whatever that 

process was that would do that.” Tr. 345:3–5, 9–11. Dr. Fine noted that the “proliferative types [of 

FGN act in that manner], but there’s no evidence [on Petitioner’s biopsy] of proliferation.” Tr. 

345:13–14. However, he further noted that “the mesangial process doesn't behave that way.” Tr. 

345:12–13. 

Dr. Fine disagreed with Dr. Ballouk that the lack of crescent formations on Petitioner’s 

biopsy would be expected because the literature only notes that a small percentage of patients have 

crescents. Tr. 347:9–17. He submitted an article by Pusey, which provides more information on 

crescentic formations in renal injury. Resp’t’s Ex. A, Tab 6. The author wrote that crescents are a 

“hallmark of inflammatory [GN] and a histologic marker of severe glomerular injury.” Id. at 1. He 

further wrote that “[c]rescentic [GN] is typically associated with the syndrome of rapidly 

progressive [GN] . . . .” Id. He explained that “[g]lomerular crescent formation appears to represent 

a nonspecific response to severe injury to the glomerular capillary wall[,]” and therefore “crescent 

formation appears to be a consequence, not a cause, of severe glomerular injury.” Id. at 1, 9. Dr. 

Fine wrote that “a currently active glomerular disease would be expected to present with cellular 

crescents on biopsy, and one that was previously active but now ‘burnt out’ will have fibrous 

crescents (or sclerosed crescents).” Resp’t’s Ex. E at 4. He explained that “crescents evolve over 

time from cellular to fibrous, and later the entire glomerulus may sclerose or scar . . . .” Id. He 

further explained that “fibrous crescents will be present for months after the initial crescent 

formation and remain as evidence of a recent active lesion . . . .” Id. Dr. Fine stated that “the 

hallmark of [rapidly progressive] . . . renal lesions is the presence of a crescent.” Tr. 349:14–15. 

Dr. Fine noted that Petitioner’s biopsy did not show crescents, but rather “[o]nly [showed] 

sclerosed glomeruli,” and he therefore concluded that Petitioner’s “disease was present for a very 

long time.” Resp’t’s Ex. E at 4. 

During his testimony, Dr. Fine opined that Petitioner’s FGN course was “typical.” Tr. 

354:7–9. He argued that Petitioner’s “course is . . . what you see in someone who has had 

longstanding [FGN] . . . .” Tr. 354:21–22. He explained that “the reason it’s longstanding is it is 

asymptomatic. You don’t get symptoms. [A patient] might get hypertension, but . . . physicians 

are saying, . . . a lot of people get hypertension, and so [the physicians] ignore it or just expect 

[hypertension] for that particular patient.” Tr. 354:23–355:2. 

Regarding onset of Petitioner’s FGN, Dr. Fine testified that he “sort of work[ed] 

backwards.” Tr. 355:8–11. He explained that Petitioner had “a very advanced lesion[,]” which he 

stated “usually takes years to develop.” Tr. 355:11–12. In addition, Dr. Fine testified that “based 

on pathology alone, [he] would . . . [estimate that] it’s been there for years.” Tr. 355:23 –24. He 

wrote that “there were no cellular crescents [present on Petitioner’s biopsy] suggestingno ongoing 

severe disease activity, and no fibrous crescents, suggesting no recent activity.” Resp’t’s Ex. E at 

4. Rather, Dr. Fine explained that Petitioner’s biopsy only revealed “sclerosed glomeruli . . . , 

which indicates that the disease was present for a very long time.” Id. He estimated that, although 

“an exact [onset] date is hard to determine, based on [his] clinical practice and experience . . . , the 

presence of global sclerosis of the diffuse nature seen on this kidney biopsy suggest that the

damage had occurred more than [five] months before the biopsy.” Id. He expounded on this belief 
42

during his testimony. He noted that “the first signs [he] see[s] of something that would go with the 

kidney disease is the hypertension, the edema, and they both occur actually very similarly around 

the middle July, August of 2011 . . . .” Tr. 355:14–17. He further stated that “the fact that the 

glomerulus that's actually visible, that isn't dead yet, that mesangial form of fibrillary supports that 

this is the way that it would have progressed, would have been over a very long period of time.” 

Tr. 356:8–13. Therefore, Dr. Fine estimated that the onset of Petitioner’s FGN occurred in 2011. 

Tr. 356:14–15.

On cross-examination, Dr. Fine explained that Dr. Lutes’ assessment that Petitioner had 

“renal insufficiency with nephrotic syndrome, [which] again, . . . has developed acutely over the 

past few months[]” did not change his opinion that Petitioner’s FGN developed over a period of 

years. Tr. 367:15–21. He opined that Dr. Lutes “was wrong[]” in his opinion because Dr. Lutes 

“can't say it's acute or chronic at [that] point.” Tr. 368:21–22. He continued, “at the time that Dr. 

Lutes” made that assessment, “all he has is one creatinine, and one creatinine doesn’t tell you 

where [Petitioner is] in the course of [her] disease.” Tr. 367:25–368:2. 

Under my questioning, Dr. Fine stated that he had seen “triggers” in patients with 

“otherwise asymptomatic kidney disease” but not in FGN patients because he’s “seen too few of 

them.” Tr. 377:25–378:5. In kidney diseases other than FGN, Dr. Fine listed infection, medication, 

and stress as “triggers . . . for kidney diseases that can make them flare or get worse.” Tr. 378:6–

9. However, Dr. Fine opined that, if Petitioner’s FGN “flared” because of an infection, for 

example, he “would have seen it on the biopsy three months later.” Tr. 379:9–12. 

I also asked Dr. Fine what he thought of Petitioner’s PCP’s statement that Petitioner’s 

biopsy “results . . . showed a lot of fibrosis, so she thinks that this may have been ongoing longer.” 

Tr. 384:5–7, 9–10 (quoting Pet’r’s Ex. 12 at 26). Dr. Fine responded that he “think[s] that’s the 

whole premise of [his] argument . . . .” Tr. 384:11–12. He explained that this “[t]ells [him 

Petitioner’s FGN] . . . wasn’t acute. This . . . was a longstanding lesion that was present for certainly 

more than five months . . . . This is years of lesion, before you get that level of fibrosis.” Tr. 

384:15–20. 

IV. Applicable Legal Standards

A petitioner in the Program is entitled to compensation if a special master determines “on 

the record as a whole” that the petitioner “has demonstrated by a preponderance of the evidence 

the matters required in the petition by [ § 300aa-11(c)(1)], and that there is not a preponderance of 

evidence that the illness, disability, [etc.] described in the petition is due to factors unrelated to the 

[vaccination].” § 300aa-13(a)(1)(A)–(B). A special master cannot award compensation “based on 

the claims of a petitioner alone, unsubstantiated by medical records or by medical opinion.” §

300(a)(1). Although a special master must consider all “diagnos[e]s, conclusion[s], [and] medical 

judgment[s] . . . regarding the nature, causation, and aggravation of the petitioner’s [condition],” 

as well as diagnostic or evaluative tests, such are not binding on the court. § 300(b)(1). When 

considering the weight to be afforded to such medical evidence, the special master must “consider 

the entire record and the course of” the petitioner’s condition. Id. 

A. Petitioner’s Overall Burden in Program Cases
43

To receive compensation under the Vaccine Act, a petitioner must demonstrate either that: 

(1) her condition is a “Table Injury,” and therefore resulted from the receipt of a covered vaccine

or vaccines within the time frame prescribed by the Vaccine Injury Table set forth at § 14, as

amended by 42 C.F.R. § 100.3; or (2) her condition is an “off-Table Injury,” one not listed on the

Table, that resulted from her receipt of a covered vaccine. See § 11(c)(1)(C); Moberly v. Sec’y of

Health & Hum. Servs., 592 F.3d 1315, 1321 (Fed. Cir. 2010); Capizzano v. Sec’y of Health &

Hum. Servs., 440 F.3d 1317, 1319–20 (Fed. Cir. 2006). Petitioner’s claim that the flu vaccination

significantly aggravated her kidney failureand glomerulonephritis does notfallwithin the Vaccine

Table. Thus, Petitionermust prove that herflu vaccination wasthe cause-in-factof the aggravation

of her condition.

To establish causation-in-fact, a petitioner must demonstrate by a preponderance of the

evidence that her vaccine was the cause of injury. § 13(a)(1)(A). A petitioner need notshow that

the vaccination was the sole cause, or even the predominant cause, of the alleged injury; showing

that the vaccination was a “substantial factor” and a “but for” cause of the injury is enough for

recovery. Pafford v. Sec’y ofHealth &Hum. Servs., 451 F.3d 1352, 1355 (Fed.Cir. 2006); Shyface

v. Sec’y of Health & Hum. Servs., 165 F.3d 1344, 1352 (Fed. Cir. 1999).108 

In Althen v. Sec’y of Health & Hum. Servs., the Federal Circuit set forth a three-pronged

test used to determine whether a petitioner has established a causal link between a vaccine and the

claimed injury. See 418 F.3d 1274, 1278 (Fed. Cir. 2005). The Althen test requires a petitioner to

set forth: “(1) a medical theory causally connecting the vaccination and the injury; (2) a logical

sequence of cause and effectshowing that the vaccination was the reason for the injury; and (3) a

showing of a proximate temporal relationship between vaccination and injury.” Id. To establish

entitlement to compensation under the Program, a petitioner is required to establish each of the

three prongs of Althen by a preponderance of the evidence. See id. (internal citations omitted).

Specifically, under the first prong of Althen, a petitioner must offer a scientific or medical

theory that answers in the affirmative the question “can [the] vaccine(s) at issue cause the type of

injury alleged?” See Pafford v. Sec’y of Health & Hum. Servs., No. 01-0165V, 2004 WL 1717359,

at *4 (Fed. Cl. Spec. Mstr. July 16, 2004), aff’d, 64 Fed. Cl. 19 (2005), aff’d, 451 F.3d 1352 (Fed.

Cir. 2006), cert. denied, 551 U.S. 1102 (2007). To satisfy this prong, a petitioner’s theory must be 

based on a “sound and reliable medical or scientific explanation.” Knudsen v. Sec’y of Health & 

Hum. Servs., 35 F.3d 543, 548 (Fed. Cir. 1994); see also Andreu v. Sec’y of Health & Hum. Servs., 

569 F. 3d 1367, 1375, 1379 (2009) (ruling that the petitioners had satisfied Althen prong one where 

their expert witness had “presented a ‘biologically plausible’ theory”). Such a theory must only be 

“legally probable, not medically or scientifically certain.” Knudsen, 35 F.3d at 548–49. 

A petitioner may satisfy this prong in a number of ways. “Reliability and plausibility of . .

. pathogenesis can be bolstered by providing evidence that at least a sufficient minority in the

medical community has accepted the theory, so as to render it credible.” Pafford, 2004 WL

1717359, at *4. Additionally, “epidemiological studies and an expert’s experience, while not

108 The Vaccine Act also requires petitioners to show by preponderant evidence that the “residual effects 

or complications” of the alleged vaccine-related injury lasted for more than six months. § 11(c)(1)(D)(i). 

It is undisputed that this six-month requirement is satisfied in this case.
44

dispositive, lend significant credence to the claim of plausibility.” Id. Medical literature published

in respected medical journals is also persuasive. Id. “However, publication ‘does not necessarily

correlate with reliability’, because ‘in some instances well-grounded but innovative theories will

not have been published.’” Id. (quoting Daubert v. Merrell Dow Pharm., Inc., 509 U.S. 579, 593–

94 (1993) (emphasis in original)). However, “a petitioner can satisfy her burden to prove a 

plausible medical theory without resort to medical literature, epidemiological studies, 

demonstration of a specific mechanism, or a generally accepted medical theory[.]” Sharpe, 964 

F.3d 1072, 1085 (Fed. Cir. 2020) (citing Andreu, 569 F.3d at 1378–79).

In addition to showing that the vaccine at issue can cause a particular injury, a petitioner

must also, underAlthen’ssecond prong, prove thatthe vaccine actually did cause the alleged injury

in a particular case. See Pafford, 2004 WL 1717359, at *4; Althen, 418 F.3d at 1278. A petitioner

does not meet this obligation by showing only a temporal association between the vaccination and

the injury; the petitioner “must explain how and why the injury occurred.” Pafford, 2004 WL

1717359, at *4 (emphasis in original) (internal citations omitted).

Although a temporal association alone is insufficient to establish causation, under the third 

prong of Althen, a petitioner must show that the timing of the injury fits with the causal theory. 

See Althen, 418 F.3d at 1278. The special master cannot infer causation from temporal proximity 

alone. See Thibaudeau v. Sec’y of Health & Hum. Servs., 24 Cl. Ct. 400, 403–04 (1991); see also 

Grant v. Sec’y of Health & Hum. Servs., 956 F.2d 1144, 1148 (Fed. Cir. 1992) (“[T]he inoculation 

is not the cause of every event that occurs within the ten[-]day period. . . . Without more, this 

proximate temporal relationship will not support a finding of causation.” (quoting Hasler v. United 

States, 718 F.2d 202, 205 (6th Cir. 1983))).

B. Standards Applicable to Significant Aggravation Claims

Petitioners must establish causation in all off-Table cases; however, petitioners may 

establish they are entitled to compensation based on a claim that vaccination significantly 

aggravated a pre-existing condition. Here, Petitioner asserts that the flu vaccine significantly 

aggravated her pre-exiting FGN. The Vaccine Act defines significant aggravation as “any change 

for the worse in a pre[-]existing condition which results in markedly greater disability, pain, or 

illness accompanied by substantial deterioration of health.” § 300aa-33(4). When a petitioner 

makes this argument, the evidentiary burden is expanded. See Loving v. Sec’y of Health and Hum.

Servs., 86 Fed. Cl. 135, 144 (2009). In Loving, the Court set forth a six-factor test, which requires 

establishing the following:

(1) the person’s condition prior to administration of the vaccine, (2) the person’s 

current condition (or the condition following the vaccination if that is also 

pertinent), (3) whether the person’s current condition constitutes a “significant 

aggravation” of the person’s condition prior to vaccination, (4) a medical theory 

causally connecting such a significantly worsened condition to the vaccination, (5) 

a logical sequence of cause and effect showing that the vaccination was the reason 

for the significant aggravation, and (6) a showing of a proximate temporal 

relationship between the vaccination and the significant aggravation.

Loving, 86 Fed. Cl. at 144. 
45

The Loving analysis requires the special master to “evaluat[e] whether the vaccine made 

the person worse than the person would have been but for the vaccination. In doing so, the natural 

course of the disease must be considered.” Locane v. Sec’y of Health & Hum. Servs., No. 99-589V, 

2011 WL 3855486 at *10 (Fed. Cl. Spec. Mstr. Feb. 17, 2011), mot. for review den’d, 99 Fed. Cl. 

715 (2011), aff’d, 685 F.3d 1375 (Fed. Cir. 2012); see also Hennessey v. Sec’y of Health & Hum.

Serv., No. 01-190V, 2009 WL 1709053, at *41–42 (Fed. Cl. Spec. Mstr. May 29, 2009), mot. for 

review den’d, 91 Fed. Cl. 126 (2010). However, a petitioner is not required “to demonstrate an 

expected outcome and that her current-post vaccination condition was worse than such expected 

outcome.” Sharpe, 964 F.3d at 1081. 

V. Analysis

A. Loving Prong One – Condition Prior to Vaccination

The parties agree that Petitioner’s FGN predated her vaccination. However, they dispute 

how long her disease had been progressing before her vaccination and whether she was 

symptomatic before her vaccination. Regarding the onset of Petitioner’s FGN, neithe r party 

proffers a precise date. Respondent’s experts opine that Petitioner was experiencing two classic 

symptoms of renal disease, hypertension and edema, beginning in July and August 2011, more 

than two years before her September 23, 2013 vaccination. Petitioner’s experts, in contrast, claim 

that her disease began, asymptomatically, shortly before her vaccination. Petitioner’s experts 

maintain that Petitioner did not experience symptoms of her FGN until after her vaccination. The 

evidence in the record demonstrates that, by a preponderant standard, Petitioner was symptomatic 

as of July 2011. Thus, by Petitioner’s September 23, 2013 vaccination, it is more likely than not 

that she had been suffering from FGN for more than two years. 

The articles submitted by Respondent, and cited by Petitioner’s expert, show that 

hypertension and edema are associated with renal disease generally, and FGN specifically. The 

Rosenstock et al. paper found that seventy-seven percent of FGN patients presented with 

hypertension and sixty-seven percent of patients presented with edema. Resp’t’s Ex. C, Tab 1, at 

4. The Nasr et al. study found that seventy-one percent of FGN patients had hypertension and fiftynine percent of patients had edema at biopsy. Resp’t’s Ex. A, Tab 5, at 4; see also Pet’r’s Ex. 50 

at 1–2, 2 n.1. The Javaugue et al. article found that seventy percent of patients at biopsy exhibited 

hypertension while fifty-six percent of patients exhibited edema. Resp’t’s Ex. A, Tab 7, at 2. These 

articles demonstrate that a substantial majority of FGN patients exhibit hypertension and/or edema 

during the course of their disease. 

Furthermore, expert opinions in the record indicate that hypertension is often the first 

symptom, and sometimes the only symptom in the early stages of renal disease. Dr. Fine stated 

that “hypertension . . . is often the first sign of kidney disease . . . .” Tr. 294:23–295:11. Dr. Fine 

asserted that a person with longstanding FGN may have longstanding FGN precisely because she 

is asymptomatic. Tr. 354:21–23. Dr. Fine indicated that an FGN patient might be asymptomatic 

except for hypertension, which doctors commonly attribute to other causes. See Tr. 354:23–355:2. 
46

The medical records first indicate that Petitioner suffered from hypertension and edema 

during a July 12, 2011 visit with Dr. Nino. See Pet’r’s Ex. 1 at 28. Petitioner again presented with 

edema on May 24, 2012, June 26, 2012, and May 30, 2013. Pet’r’s Ex. 1 at 6, 18–19. During her 

July 12, 2011 visit, Petitioner’s blood pressure reading was 138/90. Id. at 28. Her blood pressure 

during her next appointment, on August 17, 2011, was 140/86. Id. at 27. These readings were 

above Petitioner’s baseline from previous visits. See Resp’t’s Ex. A at 2. During previous visits 

with Dr. Nino on January 22, March 7, April 18, and May 31, 2011, her blood pressure readings 

were all within normal range at 118/62, 122/80, 112/66, and 118/80, respectively. Id. According 

to the more recent of the two guidelines cited by the CDC, high blood pressure is 130 mm Hg or 

higher systolic and 80 mm Hg or higher diastolic.109 Petitioner’s readings from July up to her 

September 23, 2013 vaccination fluctuated, but were generally higher than her baseline. 

Petitioner’s highest blood pressure reading during that time occurred on August 24, 2013, 

approximately one month before her vaccination. Her blood pressure on August 24, 2013, was 

176/124. Id. at 4.

While hypertension, even when accompanied by edema, may be too common to be used as 

a basis for diagnosis of any specific disease, neither symptom can be discounted once a disease 

associated with both symptoms is diagnosed. There are no other readily identified conditions or 

injuries in Petitioner’s medical history that would cause edema and high blood pressure to appear 

in such close proximity to each other. Furthermore, there is no evidence that Petitioner’s physicians 

attributed her high blood pressure or edema to any other cause. See generally Pet’r’s Ex. 1. While 

Petitioner does have a history of smoking and obesity, these are unlikely causes of her edema or

hypertension. Petitioner had a long history of obesity and smoking, but no history of hypertension 

or edema prior to 2011. Notably, Petitioner testified that she quit smoking in the fall of 2013. Tr. 

33:16–18. On January 22, 2014, she reported weight loss that had helped remedy her back pain. 

Pet’r’s Ex. 12 at 30. Yet, even after she quit smoking and reported at least some weight loss, 

Petitioner’s blood pressure was still significantly elevated at 160/110 on January 22, 2014. Id. at 

31. Dr. Fine briefly considered whether pain or anxiety could have contributed to her high blood 

pressure, but these too are unlikely. Petitioner had a history of both pain and anxiety, including 

longstanding treatment with medication. Yet, Petitioner’s blood pressure did not begin to spike 

until July 2011. Further, even if a different condition did explain Petitioner’s high blood pressure 

on one or a few occasions, that would not account for why it was consistently high in years leading 

up to her flu vaccination. Based on the expert testimony and the temporal relationships, I find it 

more likely than not that Petitioner’s hypertension and edema were early indicators of Petitioner’s 

FGN. 

That Petitioner’s FGN began years before her vaccination is further supported by her 

biopsy results. Dr. Fine testified that Petitioner’s biopsy showed “a very advanced lesion[,]” which 

“usually takes years to develop.” Tr. 355:11–12. He continued that “based on pathology alone, 

[he] would . . . [estimate that] it’s been there for years.” Tr. 355:23–24. Dr. Fine stated that the 

presence of sclerosed glomeruli on biopsy “indicates that the disease was present for a very long 

time.” Resp’t’s Ex. E at 4. 

109 See supra note 9. Petitioner’s readings are also close to qualifying as high blood pressure according to 

the older set of guidelines mentioned by the CDC. See id. 
47

Based on the foregoing, I find it more likely than not that Petitioner was suffering from and 

exhibiting symptoms of FGN, in the form of hypertension and edema, for more than two years 

prior to her vaccination. 

B. Loving Prong Two – Current, or Post-Vaccination, Condition

Petitioner’s condition post vaccination is not disputed by either party. Nearly two months 

post vaccination, Petitioner presented to the emergency room with complaints of abdominal pain, 

nausea, vomiting, and diarrhea. See Pet’r’s Ex. 3(b) at 289. During her brief hospitalization, 

Petitioner had her first high creatinine reading. See id. at 283. She was biopsied and definitively 

diagnosed with FGN on February 19, 2014. See Pet’r’s Ex. 3(a) at 62, 95. She progressed to ESRD 

requiring dialysis by June 2014. See Pet’r’s Ex. 4 at 2. At the time of the hearing, Petitioner was 

undergoing regular HD and was awaiting kidney transplantation. Tr. 28:1–3, 29:5–6. I find it more 

likely than not that Petitioner was still suffering from FGN, which later progressed to ESRD, post

vaccination. 

C. Loving Prong Three – Significant Aggravation

The parties’ most significant dispute is whether the course of Petitioner’s disease after her 

vaccination constituted a significant aggravation of her FGN. Petitioner alleges that she progressed 

to ESRD faster than what is normally expected for FGN patients. Respondent, however, argues 

that Petitioner’s FGN was more chronic in nature and that her clinical course aligned with the 

expected progression of her particular iteration of FGN. After considering the entire record, 

particularly the literature filed by the parties110 and Petitioner’s biopsy results, I find that it is more 

likely than not that the flu vaccine did not significantly aggravate the course of Petitioner’s disease. 

The articles discussed by both parties indicate various time frames in which a FGN patient 

would likely reach ESRD. Petitioner points to some of these time frames to demonstrate that 

Petitioner progressed to ESRD at an accelerated rate. Dr. Ballouk cited the Nasr et al. study, which 

found “nearly one half of patients [studied] progressing to ESRD within [four] years.” Resp’t’s 

Ex. A, Tab 5, at 9. Dr. Ballouk discussed the Jauvague et al. paper, which showed forty -eight 

percent of patients developing ESRD a median of forty-four months following diagnosis. Resp’t’s 

Ex. A, Tab 7, at 9. Dr. Ballouk further discussed the Rosenstock et al. study, which showed that 

forty-five percent of patients (including seventy-two percent of patients presenting with a 

creatinine level above 2.0) reached ESRD after a median of about two years. Resp’t’s Ex. C, Tab 

1, at 6. Asserting that he relied on the Rosenstock et al. article to form the basis of his opinions, 

Dr. Ballouk testified that forty-four percent of FGN patients “will end up on dialysis with a median 

of [twenty-four] months.” Tr. 186:24–187:1, 202:24–203:1. Dr. Ballouk later opined that the 

110 Neither party is required to file medical literature, however, it can be effective support for expert 

opinions, particularly when the opposing party does not provide rebuttal. While the undersigned has 

reviewed all of the information filed in this case, only those filings and recordsthat are most relevant to 

the decision will be discussed. Moriarty v. Sec'y of Health & Hum. Servs., 844 F.3d 1322, 1328 (Fed. Cir. 

2016) (“We generally presume that a special master considered the relevant record evidence even though 

he does not explicitly reference such evidence in his decision.”) (citation omitted); see also Paterek v. 

Sec'y of Health & Hum. Servs., 527 F. App'x 875, 884 (Fed. Cir. 2013) (“Finding certain information not 

relevant does not lead to—and likely undermines—the conclusion that it was not considered.”).
48

presence of mesangial involvement, as well as the fact that Petitioner did not have one hundred 

percent sclerosed glomeruli, indicated that she was in the MES subgroup. Tr. 274:20–275:1. Citing 

the Rosenstock et al. study, Dr. Ballouk stated that a patient in the MES subgroup would take 

eighty months to reach ESRD. Tr. 275:2–5. Dr. Ballouk, however, neglected that Petitioner falls 

into the clearly stated definition of the DS subgroup articulated in that study, which is seventy 

percent of sclerosed glomeruli. See Resp’t’s Ex. C, Tab 1, at 4. Overall, the time frames presented 

by Petitioner do not take account of the percentage of Petitioner’s glomeruli that were already 

sclerosed by the time of biopsy.

Respondent’s use of the Rosenstock et al. article to demonstrate that Petitioner’s disease 

progressed at a normal rate is very compelling. As Dr. Ballouk acknowledged, this article showed 

that the time frame to ESRD varies by histologic FGN-subgroup based on biopsy. Resp’t’s Ex. C, 

Tab 1, at 6. Specifically, as stated above, the authors of this study noted that the DS subgroup of 

FGN reached ESRD an average of seven months post biopsy. Id. at 4, 6. Furthermore, a chart 

included in the article indicates that over seventy percent of patients in the DS subgroup reached 

ESRD within two months post biopsy.111 See id. at 10.

Petitioner’s biopsy results revealed eighteen of twenty-three glomeruli were sclerosed, 

which equates to seventy-eight percent. Petitioner, therefore, falls within the DS subgroup as 

defined in the Rosenstock et al. article. She progressed from her first high creatinine finding in 

November 2013 to ESRD by June 2014. Dr. Levinson indicated that Petitioner’s creatinine, 

proteinuria, and hematuria findings on November 21, 2013, constitute “her diagnosis of a 

glomerulopathy.” See Resp’t’s Ex. C at 4. Dr. Levinson stated that counting from November 2013, 

Petitioner’s diagnosis occurred approximately seven months before she reached ESRD, which was 

consistent with the DS subgroup. Id. Even if the appropriate date to count from is that of 

Petitioner’s February 19, 2014 biopsy, that time frame of more than three months between 

Petitioner’s biopsy and ESRD is well within the range appropriate for her subgroup. 

Beside her FGN subgroup, Petitioner’s November 21, 2013 hospitalization revealed that 

she had other risk factors for reaching ESRD. The Nasr el al. article discussed by both parties 

identified “older age, higher creatinine at biopsy, higher 24-hour urine protein at biopsy, and higher 

percentage of globally sclerotic glomeruli” as “predictors of renal survival in [FGN].” Resp’t’s 

Ex. A, Tab 5, at 9. Dr. Fine concluded that it was unsurprising that Petitioner reached ESRD at the 

time she did, because age was the only risk factor that Petitioner did not have. Tr. 316:2–3; Resp’t’s 

Ex. A at 7.

I did consider that the damage to seventy-eight percent of Petitioner’s glomeruli, as well 

as the rise to high creatinine and urine protein levels, could also be evidence of an accelerated 

course following Petitioner’s vaccination. Petitioner, however, did not persuasively explain how 

Petitioner’s medical history illustrates this potential argument. Dr. Ballouk also did not 

persuasively distinguish how these indicators, present in Petitioner’s case, can be distinguished 

from a more commonly seen, slower development of FGN. He indicated during my questioning

that Petitioner’s increase in creatinine between her November 2013 reading and January 2014 

111 The average was seven months, however, because the remaining DS patients did not reach ESRD until 

twenty-four months or more post biopsy, as shown in the referenced chart. See Resp’t’s Ex. C, Tab 1, at 

10.
49

reading indicated that Petitioner’s disease was rapidly progressing. See Tr. 267:11–12. However, 

Dr. Fine persuasively rebutted this by noting that this did not dramatically impact Petitioner’s 

EGFR and explaining that, as kidney function worsens, “the creatinine rises way faster than the 

amount of kidney function you lose.” Tr. 311:11–21. Dr. Fine concluded that this did not signal 

rapid progression because “[r]apidly progressive patients lose . . . half their kidney function in 

weeks.” Tr. 311:22–24. Furthermore, Dr. Ballouk clarified that he meant that Petitioner’s disease 

was “progressive [because of the rise in Petitioner’s creatinine and proteinuria between November 

and January], and it is aggressive because she ended up on dialysis [in] four months.” Tr. 280:12–

281:1. However, the issue in this matter is whether Petitioner’s disease progressed abnormally

quickly, not whether it progressed at all. Overall, the evidence in the record does not demonstrate 

abnormal progression. 

Furthermore, Petitioner’s argument fails because her biopsy did not show any evidence 

that her FGN had progressed at an abnormal rate following her vaccination. Dr. Fine noted that 

“[eighteen] out of [twenty-three of [Petitioner’s glomeruli] . . . were dead glomeruli[,]” and that 

an additional three of Petitioner’s glomeruli displayed segmental sclerosis. Tr. 339:10–12. Dr. Fine 

stated that such sclerosis indicates that the glomeruli were “starting to scar off, but it’s probably 

an earlier stage scarring . . . .” Tr. 342:2–5. Dr. Fine continued, “in the three glomeruli that . . . he 

can actually get real information out of, there isn’t any evidence of anything that’s highly active.”

Tr. 342:12–15. Dr. Fine noted that the pathologists indicated that the glomeruli did not evince 

“crescent formation, fibrinoid necrosis, thrombosis, or endocapillary proliferation.” Tr. 342:2–4. 

Dr. Fine argued that this meant Petitioner did not suffer “rapid loss of kidney function” beginning 

in September 2013, because such rapid loss does not occur “without crescentic GN or some really 

aggressive inflammation which almost always results in crescentic formation.” Tr. 344:8–19. Dr. 

Fine stated that if Petitioner’s disease activity was bad enough to cause renal failure between 

September 2013, and Petitioner’s biopsy, the biopsy would show “evidence of whatever that 

process was that would do that.” Tr. 345:3–5, 9–11. Dr. Fine indicated that a lack of evidence 

could occur with “proliferative types, but there’s no evidence [on Petitioner’s biopsy] of 

proliferation.” Tr. 345:13–14. Dr. Fine opined that the lack of cellular crescents or fibrous 

crescents on Petitioner’s biopsy, respectively, “suggest[ed] no ongoing severe disease activity[] 

and . . . no recent activity.” Resp’t’s Ex. E at 4. 

In contrast, Dr. Ballouk opined that “the lack of crescents on [Petitioner’s] biopsy does not 

mean that [Petitioner’s] vaccination did not aggravate her disease.” Pet’r’s Ex. 50 at 2. Dr. Ballouk 

indicated that only around thirteen percent of biopsies of patients with Petitioner’s disease reveal 

crescents. Tr. 198:2–7. He stated that Petitioner’s “active disease could have ceased prior to 

biopsy.” Pet’r’s Ex. 50 at 2. 

Overall, I find Dr. Fine’s explanation of Petitioner’s disease progression more compelling 

than Dr. Ballouk’s. Dr. Ballouk estimated that Petitioner’s disease began around September 2013 

and was aggravated by her vaccination that same month. Dr. Ballouk argued that Petitioner

manifested symptoms of her disease by November 2013, about two months after his proposed 

onset. In contrast to the acute progression suggested by Dr. Ballouk, Dr. Fine, argued that 

Petitioner’s disease progression was more chronic in nature. He estimated that Petitioner’s disease 

began in 2011 because Petitioner was experiencing symptoms, in the form of hypertension and 

edema, at that time. 
50

Dr. Ballouk estimated the onset of Petitioner’s FGN based on the notion that her November 

2013 gastrointestinal issues were sequela of her FGN. Dr. Ballouk then concluded that Petitioner 

reached ESRD at an accelerated rate from September 2013, but he did not point to any medical 

literature to explain how this can occur. The lack of literature is not fatal, however. Due to the rare 

nature of vaccine-caused injuries, Petitioner is not required to submit medical literature in support 

of her medical theory. Dr. Ballouk also did not persuasively support his theory regarding onset by 

using Petitioner’s medical record or other corroborative evidence. As previously discussed, Dr. 

Ballouk noted the difference between Petitioner’s creatinine levels in November 2013 an d January 

2014, but he did not present persuasive evidence that this represented abnormal progression. In 

this case, with respect to FGN symptomatology, I must consider Dr. Ballouk’s opinion that is 

substantially unsupported, versus Dr. Fine’s theory that effectively relies on supporting literature 

and explains Petitioner’s medical record.

Dr. Fine’s reliance on medical literature to link edema and hypertension to kidney disease 

is persuasive. The literature helped to explain that hypertension and edema are often the first 

symptoms in an otherwise asymptomatic early phase of disease. Dr. Fine then related this 

information to Petitioner’s medical records and explained the progression of Petitioner’s disease.

Dr. Fine explained that he believed Petitioner was already in stage four of her disease by her 

November 21, 2013 hospitalization, based on her elevated creatinine levels on that date. See Tr. 

309:10–22. Dr. Fine maintained this assertion even when accounting for Dr. Ballouk’s suggestion 

that Petitioner’s creatinine levels were elevated on that date due to dehydration. See Tr. 310:9–14.

Dr. Ballouk explained that active disease could have ceased prior to biopsy, Pet’r’s Ex. 50 

at 2, but he did not explain how crescents could have appeared and subsequently disappeared all 

within a few months of the rapid acceleration of her disease. Furthermore, Dr. Ballouk failed to 

explain how rapid progression of Petitioner’s disease before biopsy would not result in crescents 

or any other indicators of disease activity. Dr. Ballouk noted that the majority of FGN biopsies do 

not reveal crescents. See Tr. 198:2–18. However, he did not explain under what circumstances 

they would appear or distinguish those cases from Petitioner’s. Dr. Fine did, however, explain that 

the three segmentally sclerosed glomeruli he identified would have revealed crescent formation if 

Petitioner’s disease had been recently active. See Resp’t’s Ex. E at 4. Dr. Fine asserted that the 

biopsy would have revealed recent activity, in the form of fibrous crescents, even if her disease 

had “burnt out” prior to her February 19, 2014 biopsy. Id. Petitioner did not rebut this.

I am not persuaded by Dr. Ballouk’s assertion that Petitioner’s clinical course was 

significantly aggravated by the flu vaccine, largely because he did not effectively use her medical

record to identify indicators of disease exacerbation. Dr. Fine provided strong support for his 

assertions in the record and through medical literature that were not rebutted by Dr. Ballouk. I 

conclude that Petitioner did not establish it is more likely than not that her disease was highly 

active following her September 23, 2013 vaccination, or because of it. Further, Petitioner’s biopsy

did not reveal persuasive evidence to support Petitioner’s claim of an accelerated course. Without 

additional support, I cannot conclude that, by a preponderant standard, Petitioner’s vaccination 

significantly aggravated her injury. 

D. Loving Prong Four/Althen Prong One – Medical Theory
51

Dr. Gershwin presented a theory whereby “the cytokine response following the [flu] 

vaccination would have accelerated [Petitioner’s] [FGN] and made it worse.” Pet’r’s Ex. 19 at 1. 

For the reasons discussed below, Petitioner’s theory fails to meet her burden under Loving prong 

four/Althen prong one.

Dr. Gershwin testified that the flu vaccine produces cytokines. Tr. 67:14–23. He went on 

to identify some of these cytokines and explained that cytokines can act locally or systemically. 

See Tr. 62:23, 66:8–16. Dr. Gershwin continued that cytokines produced in response to a 

vaccination travel through the body. Tr. 69:3–12. He opined that cytokines produced in response 

to a vaccination that travel throughout the body could then interact with the kidneys, especially if 

the vaccination occurred “in the early phase of disease.” Tr. 70:1–5. Dr. Gershwin stated that 

cytokines produced following a vaccination travel around the body because they “get in the sera . 

. . .” Tr. 69:3–9. He explained that someone in the early phases of disease “was a susceptible host” 

because the pro-inflammatory cytokines “would exacerbate an ongoing inflammatory process in 

the kidney . . . .” Tr. 78:16–22, 79:15–16. 

Petitioner’s discussion of vaccine-induced cytokines and her attempt to link them to her 

disease do not constitute a sufficient medical theory. Petitioner fails to account for the fact that 

many different types of cytokines are typically present in the body and stem from a variety of 

causes. Although Dr. Gershwin stated that some of the “key” cytokines produced in response to 

the flu vaccine are from the interferon family, see Tr. 67:17–23, he did not clarify the role of 

interferons in his theory. In particular, he did not explain whether interferons were the only types 

of cytokines involved in the reaction he alleged. Ultimately, Dr. Gershwin’s assertions that 

different people will produce different cytokines in response to the flu vaccine and that there are 

many different cytokines that can be produced in such a response equivocate his attempt to identify 

a “key” family of cytokines. An assertion that vaccine-induced cytokines caused the significant 

aggravation of a disease, without a specific or even general explanation of the types of cytokines 

involved and how they could aggravate the condition, is too general to constitute a sufficient 

medical theory. See Jaafar v. Sec’y of Health & Hum. Servs., No. 15-267V, 2018 WL 4519066 at 

*5 (Fed. Cl. Spec. Mstr. Aug. 10, 2018) (determining that a petitioner did not establish an adequate 

medical theory that vaccine-induced cytokines triggered a condition when the “cytokine theory 

[was] conclusory and not persuasively supported[]”); Cf. Doe/11 v. Sec’y of Health & Hum. Servs., 

No. 99-212V, 2008 WL 4899356 at *9 (Fed. Cl. Spec. Mstr. Oct. 29, 2008) (decision on remand) 

(concluding that the petitioners satisfied the first prong of Althen when they explained the two 

particular cytokines involved and explained how their release resulted in the injury in question), 

mot. for review den’d, 87 Fed, Cl. 1 (2009), aff’d, 601 F.3d 1349 (Fed. Cir. 2012), cert. den’d, 562 

U.S. 1029 (2010).

Dr. Levinson opined that “it is highly unlikely that the cytokine response to the inactivated 

seasonal [flu] vaccine [received] by [Petitioner] reached a level of magnitude to deleteriously 

impact organs distant to the injection site.” Resp’t’s Ex. C at 5. Dr. Levinson stated that the flu 

virus may induce a “cytokine storm” causing lung inflammation and other organ dysfunction. Id. 

However, he maintained that “there is not credible scientific evidence” that vaccines are capable 

of inducing a cytokine storm. Id. Petitioner does not allege that she suffered from a cytokine storm 
52

as a result of her vaccine. Cytokine storm is a catastrophic autoimmune response, and there is not

evidence of that occurring in Petitioner’s case.

Petitioners are not required to submit the exact biological mechanism for a vaccine-caused 

injury. However, any theory that is asserted should be applicable to the vaccination given and the 

disease Petitioner suffers from. Petitioner’s purported mechanism amounts to little more than a 

vague declaration that there are proteins (cytokines) that appear post-vaccination (produced as 

result of an immune response triggered by the vaccine), travel to the kidneys (because the kidneys 

are already diseased), and tell the kidney to attack itself (for reasons unknown). Petitioner has not 

asserted that the flu vaccination elicited any specific cytokines in her case. In fact, Dr. Gershwin 

stated that the types of cytokines triggered by the flu vaccine vary from person to person. Tr. 

67:17–23. Furthermore, there is no explanation of why this vaccine would produce cytokines 

triggered by pre-existing kidney disease. Dr. Gershwin submitted numerous articles to illustrate 

the role pro-inflammatory cytokines play in renal injury. However, none of these articles were 

specific to FGN. And, as Dr. Levinson explained, the articles submitted all discuss proinflammatory cytokines that are produced in the kidneys rather than elsewhere in the body. The 

fact that these cytokines are produced in the kidneys provides a logical explanation for why they 

would target an already diseased kidney. Dr. Gershwin did not link any of these cytokines to FGN 

or explain why they are instructive to Petitioner’s case. Therefore, the articles are unhelpful in 

explaining how cytokines produced locally in response to a vaccination would travel to Petitioner’s 

kidneys and lead to organ damage.

Again, I must note that Petitioner is not required to provide a specific biological 

mechanism. However, given the ubiquitous nature of cytokines in the body, it cannot be enough 

to simply say “cytokines did it.” Petitioner has not provided sufficient evidence that cytokines of 

any kind impact FGN. Importantly, Petitioner has not provided reliable medical evidence that 

vaccine-induced cytokines can cause or aggravate inflammation or injury at a distant site.

Furthermore, Dr. Gershwin opined during his testimony that FGN is an immunological 

disease but conceded that there has not been a definitive characterization found in the literature. 

See Tr. 70:24–72:6. In addition, Dr. Gershwin submitted numerous studies that discuss the 

immunological components of the disease. Taken together, these articles do support the contention 

that FGN is an immunologic disease. Neither of Respondent’s experts rebutted this contention, 

and Dr. Levinson even testified under the assumption that FGN may be an immunological disease 

in order to rebut other parts of Petitioner’s theory. See Tr. 115:25–116:11. Therefore, I find that 

FGN is an immunological disease.

However, Petitioner has failed to establish by a preponderant standard that inactivated 

vaccines can cause exacerbation of underlying autoimmune diseases, regardless of whether they 

are active or stable. Dr. Levinson provided two articles that supported that such vaccines are 

considered safe for people with AIRDs. See Resp’t’s Ex. C, Tabs 2–3.The authors of both of those 

articles acknowledged that research into the issue is incomplete. However, both articles show that 

existing studies have not established a link or causal relationship between vaccines and disease 

flares in AIRD patients. Furthermore, Dr. Levinson stated during his testimony that, if Petitioner’s 

theory was correct, then based on the amount of people who are vaccinated each year with the 

inactivated flu vaccine, who have underlying autoimmune diseases, there should be more 
53

documented cases and studies showing the aggravating effects of the vaccine. See Tr. 119:11–13, 

120:12–19. I conclude that although FGN is an immunologic disease, this does not clarify 

Petitioner’s purported theory.

Based on the foregoing, I find that Petitioner has not presented preponderant evidence that 

the flu vaccine can significantly aggravate FGN. 

E. Loving Prong Five/Althen Prong Two – Actual Causation

Petitioner has failed to present preponderant evidence that the flu vaccine she received 

significantly aggravated her FGN. As I have already discussed, Petitioner did not meet her burden 

under Loving prong three. 

Furthermore, although Petitioner’s purported theory is that her FGN was aggravated by a 

vaccine-induced cytokine response, Dr. Gershwin does not point to evidence in Petitioner’s 

medical record to support his contention that she suffered from a vaccine-induced cytokine 

response. Dr. Gershwin stated that the “[flu] vaccine elicits a rigorous cytokine response and this 

response begins within hours of the vaccination.” Pet’r’s Ex. 19 at 3. Dr. Gershwin, however, did 

not explain what “a rigorous cytokine response” would look like or how it would have manifested 

in Petitioner’s case. As Dr. Levinson noted, the medical records do not indicate cytokine testing 

or any evidence that Petitioner suffered from a cytokine storm. 

Based on the foregoing, I find that Petitioner has failed to meet her burden under Loving 

prong five/Althen prong two. 

F. Loving Prong Six/Althen Prong Three – Temporal Relationship

Dr. Gershwin specified that “if the time of [FGN] onset was distant from the vaccination, 

then [he] would not hold” the opinion that the flu vaccine exacerbated Petitioner’s FGN. Tr. 58:8–

9. He indicated that his position would be inappropriate if the onset of Petitioner’s FGN was more 

than six weeks before her vaccination. See Tr. 83:9–10. I have already concluded by a preponderant 

standard that Petitioner’s FGN predated her vaccination by more than two years. Therefore, relying 

on Petitioner’s own expert, Petitioner’s course exhibits an inappropriate time frame for the flu 

vaccine to significantly aggravate her FGN. Accordingly, Petitioner has failed to meet her burden 

under Loving prong six/Althen prong three. 

VI. Conclusion

Based on the foregoing, I find that Petitioner has failed to show by preponderant evidence 

that the flu vaccine she received on September 23, 2013, significantly aggravated her FGN. 

Therefore, her petition is hereby DISMISSED.

In the absence of a motion for review filed pursuant to RCFC Appendix B, the clerk of the 

court SHALL ENTER JUDGMENT in accordance with the terms of the above decision. 112

112 Pursuant to Vaccine Rule 11(a), entry of judgment is expedited by the parties’ joint filing of a notice 

renouncing the right to seek review.
54

IT IS SO ORDERED.

 s/Herbrina D. Sanders

 Herbrina D. Sanders

Special Master