Clinical trial NCT03106298: Iron Deficiency and FGF23 Regulation in CKD and HF
Official title: Iron Deficiency and Fibroblast Growth Factor 23 Regulation in Chronic Kidney Disease and Heart Failure
Study type: OBSERVATIONAL
Overall status: COMPLETED
Conditions: Chronic Kidney Diseases
Chronic Heart Failure
Iron Deficiency Anemia
Keywords: Iron Deficiency
Fibroblast Growth Factor 23
Phosphate
Lead sponsor: Northwestern University
Sponsor class: OTHER
Collaborators: name: National Kidney Foundation, United States
First posted: 2017-04-10
Enrollment: 77
Sex: ALL
Minimum age (years): 18
Standard ages: ADULT
OLDER_ADULT
Accepts healthy volunteers: yes
Observational model: OTHER
Time perspective: PROSPECTIVE
Sampling method: NON_PROBABILITY_SAMPLE
Study population: All patients with iron deficiency anemia will be enrolled (those without CKD or HF, those with CKD only, those with HF only, and those with CKD/HF). They will be given iron sucrose as routine care for treatment of their iron deficiency anemia.

Brief summary: This study investigates the effects of intravenous (IV) iron sucrose therapy on blood levels of Fibroblast Growth Factor 23 (FGF23, a protein that regulates the amount of phosphate in the body) in iron deficiency anemia in healthy participants, participants with Congestive Heart Failure (CHF, where the heart does not pump adequate blood supply to the body), participants with Chronic Kidney Disease (CKD, where the kidney function is reduced), and participants with CKD and CHF.

Detailed description: Iron is a key part of our red blood cells which bring oxygen to our body's tissues. Without iron, our blood cannot carry oxygen. The body normally gets iron through diet and it also re-uses iron from old red blood cells. When iron stores are low, patients get iron deficiency anemia. This can happen because patients lose more red blood cells and iron than the body can replace, the body does not do a good job at absorbing iron from the diet, or the body is able to absorb iron but patients are not getting enough iron from their diets. Many patients with chronic diseases such as CKD and CHF also have iron deficiency anemia.

Iron deficiency may also cause a hormone in the body named FGF23 to rise. FGF23 is a hormone that is made in bone and has an important role in the heart and kidney. When the kidneys are not working properly, as in CKD, or when the heart is not pumping correctly, as in CHF, FGF23 levels in the blood go up. Many patients with CKD or CHF also have low levels of iron. In these cases, FGF23 levels may rise even more. Too much FGF23 in the blood may lead to an increased risk of heart problems and accelerate loss of kidney function. The best way to control FGF23 levels in the blood in CKD and CHF is not known.

The investigators are conducting a 6-week iron deficiency anemia study on healthy individuals,individuals with CKD, and individuals with CHF to find out if treating iron deficiency anemia with intravenous iron sucrose therapy can safely and successfully lower FGF23 levels. Iron sucrose has been shown to lower FGF23 in animal models. The short term effects of iron sucrose on FGF23 levels in CKD and CHF are not known.

Eligibility criteria: Inclusion Criteria:

* Age ≥ 18 years old
* Ability to understand and the willingness to sign a written informed consent.
* Iron Deficiency Anemia, as defined by
* Ferritin level \< 100 ng/ml or
* Transferrin saturation \<20% with ferritin 100-350 ng/ml and
* Hemoglobin \< 12 g/dl

Exclusion Criteria:

* Hypersensitivity to any component of iron sucrose
* Malignancy within 5 years
* End stage renal disease or kidney transplantation
* Erythropoiesis stimulating agents
* Red blood cell transfusions within last 60 days
* Current radiotherapy or chemotherapy
* Aspartate aminotransferase (AST) or alanine aminotransferase (ALT) levels greater than 1.5 times normal
* Hemochromatosis
* Chronic digestive diseases
* Pregnancy or nursing
* Active alcohol or drug abuse
* Uncontrolled hypertension
* Active infection
* Hospitalization in the 4 preceding weeks
* Concomitant use of antibiotics
* Concomitant use of immunosuppression
* Inability to consent.
* Conditions, in which of the opinion of the investigator, make participation unacceptable

Primary outcomes:
measure: Change in c-terminal FGF23 measurements
timeFrame: Weekly x 6 weeks, 1 longitudinal measurement at 3 months
measure: Change in Intact FGF23 measurements
timeFrame: Weekly x 6 weeks, 1 longitudinal measurement at 3 months
Secondary outcomes:
measure: Change in Parathyroid Hormone
timeFrame: Weekly x 6 weeks, 1 longitudinal measurement at 3 months
measure: Change in Phosphate (mg/dl)
timeFrame: Weekly x 6 weeks, 1 longitudinal measurement at 3 months
measure: Change in Serum creatinine
timeFrame: Weekly x 6 weeks, 1 longitudinal measurement at 3 months
measure: Change in 1,25 dihydroxyvitamin D
timeFrame: Weekly x 6 weeks, 1 longitudinal measurement at 3 months
measure: Change in C-reactive protein
timeFrame: Weekly x 6 weeks, 1 longitudinal measurement at 3 months
measure: Change in Ferritin Measurement
timeFrame: Weekly x 6 weeks, 1 longitudinal measurement at 3 months
measure: Change in Iron Measurement
timeFrame: Weekly x 6 weeks, 1 longitudinal measurement at 3 months
measure: Change in Transferrin Saturation
timeFrame: Weekly x 6 weeks, 1 longitudinal measurement at 3 months
measure: Change in Hemoglobin Measurement
timeFrame: Weekly x 6 weeks, 1 longitudinal measurement at 3 months
Other outcomes:
Locations:
city: Chicago
country: United States
facility: Northwestern University
state: Illinois
Study officials:
affiliation: Northwestern University
name: Rupal Mehta, MD
role: PRINCIPAL_INVESTIGATOR
References: