In this question I have more doubts as to which is the correct answer, since we must interpret which is the most useful test, with which we can obtain more performance. However, this situation also depends on the radiology services of each center and their preferences. I will focus on the urological part, leaving aside the rest of the symptomatology. - Abdominal X-ray is the first imaging study to be performed because it is fast, simple and practically innocuous (except in children and pregnant women). 90% of the stones are radiopaque and therefore visible, but the sensitivity of this test, used in isolation, decreases to 45-59%. It is a mandatory test in any suspicion of colic pain. However, it has a lower yield than the others. Although the urological history speaks of uric lithiasis (radiotransparent), with an acid pH that reaffirms the diagnosis of uric origin, we can never rule out calcium oxalate lithiasis that can appear synchronously. - IVUS seems to me to be one of the best performing options. It will give us diagnostic clarity of obstruction, its magnitude and its renal repercussions. It has long been considered the examination of choice for the study of patients with renal lithiasis. It is a test with high sensitivity and specificity (87-90% and 94-100%, respectively), relatively innocuous, and available in all hospitals. It informs us of the number, size, shape and location of the stone, as well as the functional status of the affected kidney. - Contrast-enhanced CT seems to me to be the most efficient option. It serves to discover lithiasis that other tests cannot find and gives us a global image of the rest of the structures. Great performance but also more expensive, more time, more radiation. It has been confirmed as a high sensitivity and specificity scan, surpassing previous tests (94-100% and 92-100%, respectively, for the detection of ureteral calculi) and with its numerous advantages it has become the reference test and is expected to replace IVUS and ultrasound worldwide. It performs a helical scan with 5 mm slices allowing the detection of stones up to 2 mm. With the administration of contrast, it allows the evaluation of renal function. - Ultrasound is a fast, cheap and innocuous test, but very radiologist-dependent. It gives great renal information on obstructive repercussions, but less quality in terms of finding a lithiasis. Ultrasonography only detects calculi larger than 4 mm, located in the pyelo-ureteral junction or the uretero-vesical junction, while the lumbar and pelvic ureter is not very accessible due to the interposition of the intestinal loops. Therefore, ultrasound performed in isolation is not very sensitive (20-45%) for the detection of calculi, but associated with simple abdominal radiography increases its sensitivity and specificity. - Doppler echocardiography has no use in urological diagnosis. My answer would be CT with ev contrast and excretory phase (answer (c)), in terms of performance, sensitivity and specificity. There are radiology services more skilled or predisposed to one or the other. Without forgetting that abdominal X-ray should always be done in the suspicion of colic.

A 45-year-old male patient with a history of uric lithiasis with repeated expulsive nephritic colic for 25 years, comes to the ED referring palpitations and intense right lumbar pain since 2 hours before. Urinalysis showed a pH of 5.5 and leukocyturia without proteinuria. The ECG confirms a previously unknown atrial fibrillation. Blood biochemistry shows a creatinine of 0.9mg/dl, a calcium of 11mg/dl and an LDH of 950 U/l. What is the most useful diagnostic maneuver to perform?

Acute renal embolism. Forty-four cases of renal infarction in patients with atrial fibrillation.

Acute renal embolus is rarely reported in the medical literature; thus, accurate data regarding presentation, laboratory tests, diagnostic techniques, and treatment are lacking. To better define this condition, we examined the medical records of all patients admitted to Kaplan Medical Center and Sheba Medical Center in central Israel from 1984 to 2002 who had a diagnosis of renal infarction and atrial fibrillation. We noted demographic, clinical, and laboratory parameters; method of diagnosis; treatment received; and patient outcome. We identified 44 cases of renal embolus: 23 females and 21 males, with an average age of 69.5 +/- 12.6 years. Thirty (68%) patients had abdominal pain, and 6 (14%) had a previous embolic event. Nine patients were being treated with warfarin on admission, 6 (66%) of whom had an international normalized ratio (INR) < 1.8. Hematuria was present in 21/39 (54%), and 41 (93%) patients had a serum lactate dehydrogenase (LDH) level > 400 U/dL. The mean LDH was 1100 +/- 985 U/dL. Diagnostic techniques included renal isotope scan, which was abnormal in 36/37 cases (97%); contrast-enhanced computed tomography (CT) scan, which was diagnostic in 12/15 cases (80%); and ultrasound, which was positive in only 3/27 cases (11%). Angiography was positive in 10/10 cases (100%). Twenty-three (61%) of 38 patients had normal renal function on follow-up. The 30-day mortality was 11.4%. Renal embolus was diagnosed mainly in patients aged more than 60 years, some of whom had a previous embolic event. Most of those receiving anticoagulant therapy had a subtherapeutic INR. Abdominal pain was common, as well as hematuria and an elevated LDH. These patients are at risk of subsequent embolic events to other organs. The most sensitive diagnostic technique in this population is a renal isotope scan, but contrast-enhanced CT scan requires further assessment.

Heightened suspicion and rapid evaluation with CT for early diagnosis of partial renal infarction.

Although renal infarction has been well studied and clearly defined, it remains greatly underdiagnosed, resulting in significant morbidity. Acute segmental renal infarction is a diagnosis even more problematic, as the problem can appear insidiously and masquerade as other entities including stone, infection, and even tumor. The clinical manifestations and evaluation of partial renal infarction in our patients were reviewed. Seven patients presenting to the emergency department who were subsequently found to have partial renal infarction were identified from the 5-year records of a single institution. Patients were evaluated for presenting complaints, physical findings, temperature, and blood pressure. Laboratory analysis consisted of a complete blood count (CBC); measurements of creatinine, lactate dehydrogenase (LDH), aspartate transaminase/alanine transaminase (AST/ALT), and alkaline phosphatase; and urinalysis. The sequence of the work-up was recorded, as well as time to diagnosis. The etiology of infarction was identified for all patients. All seven patients were eventually discovered to have partial renal infarction as a result of dysrhythmia (N = 4), mural thrombus (N = 2), or septic emboli (N = 1). The average time to diagnosis was 65.2 hours with a range of 9.5 to 168 hours. The chief complaint was flank pain (N = 3), nonspecific abdominal pain (N = 2), left lower-quadrant pain (N = 1), and mental status change (N = 1). The presenting signs and symptoms included abdominal tenderness (N = 4), nausea and vomiting (N = 4), temperature >100.5 degrees F (N = 3), and hypertension (N = 3). Laboratory studies revealed a white cell count >11,000/microL in six, microhematuria in four, proteinuria in four, elevated LDH in all patients, elevated AST/ALT in two, and elevated alkaline phosphatase in one. The work-up varied by presentation, but definitive diagnosis was made by CT in all five patients scanned and by angiography in two. Angiography confirmed the CT findings in four of the five patients. In evaluating partial renal infarction, a strong clinical suspicion is necessary. We found a history of dysrhythmia or other cardiac disease, the presence of abdominal or flank pain, fever with an elevated white cell count, and an elevated LDH to be clinically significant, and their presence should alert the clinician to the possibility of renal infarction. Once a degree of suspicion exists, early evaluation with CT should speed the diagnosis and effect decreased morbidity.

The clinical spectrum of acute renal infarction.

Acute renal infarction is an oft-missed diagnosis. As a result, its true incidence, although presumed to be low, is actually unknown. Surprisingly, the medical literature on the subject, other than anecdotal case reports, is scarce. To increase physician awareness of the diagnosis and to identify predictive clinical and laboratory features of the entity. Between 1 November 1997 and 31 October 2000, 11 cases of acute renal infarction in 10 patients were diagnosed in our center by contrast-enhanced computerized tomography. The medical charts of these patients were reviewed regarding risk factors, clinical presentation, possible predictive laboratory examinations, and outcome. During the 36 month observation period, the incidence of acute renal infarction was 0.007%. The mean age of the patients (5 men and 5 women) was 67.4 +/- 21.1 (range 30-87 years). In four cases the right and in five the left kidney was involved; in the other two cases bilateral involvement was seen. In 7/10 patients, an increased risk for thromboembolic events was found. Six had chronic atrial fibrillation and one had a combined activated protein C resistance and protein S deficiency. Three patients had suffered a previous thromboembolic event. Two cases were receiving anticoagulant therapy with an INR of 1.6 and 1.8, respectively. On admission, flank pain was recorded in 10/11, fever in 5 and nausea/vomiting in 4 cases. Hematuria was detected in urine reagent strips in all cases. Serum lactate dehydrogenase and white blood cell count were elevated in all cases (1,570 +/- 703 IU/L and 12,988 +/- 3,841/microliter, respectively). In no case was the diagnosis of acute renal infarction initially entertained. The working diagnoses were renal colic in 2, pyelonephritis in 3, renal carcinoma, digitalis intoxication, and suspected endocarditis in one patient each, and an acute abdomen in 3. Time from admission to definitive CT diagnosis ranged from 24 hours to 6 days. Three patients were treated with intravenous heparin and another with a combination of i.v. heparin and renal intra-arterial urokinase infusion with, in the latter case, no recovery of function of the affected kidney. With the exception of this one patient (with a contralateral contracted kidney) who required maintenance dialysis, in all other cases serum creatinine levels remained unchanged or reverted to the baseline mean of 1.1 mg/dl (0.9-1.2). Acute renal infarction is not as rare as previously assumed. The entity is often misdiagnosed. Unilateral flank pain in a patient with an increased risk for thromboembolism should raise the suspicion of renal infarction. In such a setting, hematuria, leucocytosis and an elevated LDH level are strongly supportive of the diagnosis.

Case 294.

History A 50-year-old woman presented to the emergency department of our hospital with a 2-day history of lower limb pain associated with unusual asthenia and diffuse arthralgia over the past 3 weeks. She was a native of Guinea and had lived in France for most of her life, working as a personal care assistant. Her only medical history of note was an occurrence of fetal death at 12 weeks gestation when she was 35 years old. She had bilateral lower limb swelling, without changes in skin temperature or color. All proximal and distal arterial pulses were felt. General physical examination findings were otherwise unremarkable. Her laboratory tests showed a decreased hemoglobin concentration of 8.9 g/dL (normal range, 12-16 g/dL), a decreased platelet count of 45 × 10<sup9</sup/L (normal range, 150-400 × 10<sup9</sup/L), a C-reactive protein level of 158 mg/L (normal range, <5 mg/L) and a d-dimer level of 2000 mg/L (normal range, <500 mg/L). Compression US of the lower limbs revealed bilateral calf vein thrombosis involving the fibular and posterior tibial veins. Curative anticoagulation using low-molecular-weight heparin (enoxaparin, subcutaneous injection of 100 units per kilogram of body weight twice a day) was started. The day after the start of anticoagulation therapy, the patient reported dyspnea and acute chest and abdominal pain. Her vital signs were assessed, and she had elevated blood pressure and increased heart rate and respiratory rate, but she remained afebrile. Her cardiac auscultation was unremarkable, besides tachycardia. Skin examination revealed small areas of necrosis on the fingertips of her right hand. Laboratory studies were repeated and showed an increase in serum creatinine level from a baseline value of 0.49 mg/dL to a new value of 1.01 mg/dL (normal range, 0.6-1.1 mg/dL), an apparition of low-grade proteinuria of 0.43 g per day (normal range, <0.3 g/day), and a high serum troponin level of 1066 ng/L (normal range, <14 ng/L), whereas electrocardiography showed no ST segment modification and echocardiography revealed a moderately altered left ventricular ejection fraction (45%). There was no coronary occlusion seen at emergency coronarography. Contrast-enhanced CT of the chest, abdomen, and pelvis was performed (Figs 1, 2) together with cardiac MRI (Figs 3, 4).

Lanthanum carbonate has a radiopaque appearance on the plain abdominal radiography.

An 84-year-old woman presented to her local emergency department for abdominal pain. Her medical history included hemodialysis in the treatment of chronic renal failure, Parkinson's disease, chronic atrial fibrillation, chronic constipation, appendicectomy and cholecystectomy. The patient complained of diffuse abdominal pain for 4 days, associated with nausea and vomiting in the last 24 hours. Physical examination revealed a soft and depressible abdomen, diffusely painful, without signs of peritoneal irritation. A digital rectal exam revealed large amount of stool in the rectal vault without palpable masses. Blood tests showed a creatinine level of 2.7 mg/dl due to chronic renal failure and the plain abdominal radiography revealed a dolichocolon completely contrasted. The patient denied the realization of any medical imaging-proofs with oral or rectal contrast. Reviewing home treatment, the patient was taking lanthanum carbonate (2 tablets of 750 mg per day) since 1 month ago, a drug that contrasts the digestive tract. Appreciating contrast in the colon, intestinal subocclusion was excluded and the clinical picture was attributed to her chronic constipation. In conclusion, it should be noted that lanthanum carbonate contrasts the digestive tract, with radiopaque appearance on the plain abdominal radiography and without any pathological significance.

ED presentations of acute renal infarction.

The objective of the study was to investigate initial clinical characteristics that can suggest an early diagnosis of patients with acute renal infarction presenting with flank and/or abdominal pain in the emergency department (ED). From January 1, 1996, through December 31, 2005, 20 adult patients with renal infarction diagnosed by contrast-enhanced computed tomography in the ED were enrolled. Medical records, including demographic data, risk factors for thromboembolism, initial clinical presentations, laboratory data, treatment programs and outcomes, were retrospectively reviewed and analyzed. Mean patient age was 60.3 years (range, 21-80). The estimated incidence of renal infarction was 0.004% (20 of 481,540) among the ED census. The median time of onset of symptoms before the ED visit was 31 hours (range, 1-285). Eighteen patients (90%) had a history of more than 1 risk factor for thromboembolic events. In clinical presentations, all the patients had either abdominal or flank pain and tenderness. Nineteen patients (95%) had an elevated serum lactate dehydrogenase level with a mean +/- SD of 812.1 +/- 569.4 U/L. Sixteen patients (80%) presented with the triad--persisting flank or abdominal pain/tenderness, elevated serum lactate dehydrogenase level, and proteinuria. Among all 20 patients, 10 patients (50%) were diagnosed as having renal infarction at the initial ED visit. No specific clinical characteristics could be identified to distinguish those patients diagnosed early and those with delayed diagnosis. All 20 patients received medical treatment with coumadin, which was given in combination with heparin treatment in 11, peripheral intravenous and/or local intra-arterial thrombolytics with urokinase in 5, and mitral valve replacement in 1. No patient died. Although 4 patients had a mildly elevated serum creatinine level (>1.5 mg/dL) during hospitalization, none of them needs dialysis after more than 1 year of follow-up. In this study, we delineated specifically clinical features for emergency physicians to raise their suspicion index for an early diagnosis of patients with renal infarction, a disease which is uncommon and is usually delayed or missed at initial ED presentation.

Renal Infarction -- Introduction

The diagnosis of renal infarction should be considered in patients who develop sudden abdominal or flank pain with reduced renal function, hematuria, elevated LDH, or proteinuria and who do not have urolithiasis or any other diagnosable explanation for their symptoms. The chances increase if the patient has cardiac disease, especially atrial fibrillation, or is older. Since many of these patients will receive an initial non-contrast abdominal CT scan, progressing immediately to a contrast-enhanced study if the original CT scan is negative is quite reasonable and facilitates arriving at the correct diagnosis much more rapidly. [6] [7] This is essential for initiating revascularization therapy promptly, which optimizes renal functional recovery.

Renal Infarction -- Evaluation -- Imaging

An EKG should be done to look for atrial fibrillation in all patients diagnosed with renal infarction. A transthoracic or transesophageal echocardiogram can evaluate the possibility of cardiac thromboembolic disease and thrombi. A careful assessment of coagulation disorders should be performed if cardiac and renal arterial pathology have been eliminated as causative factors of renal infarction or if surgical revascularization is being considered. [45] There are clinical factors that might help distinguish renal infarction from renal colic. [46] They include: Age >70 years with no previous history of nephrolithiasis Atrial fibrillation C-reactive protein >0.23 mg/dL Serum LDH >500 IU/L (especially with normal serum aminotransferases) More likely to be diabetic and hypertensive Negative urinalysis for RBCs Negative non-contrast CT scan

Intravenous urography revisited in the age of ultrasound and computerized tomography: diagnostic yield in cases of renal colic, suspected pelvic and abdominal malignancies, suspected renal mass, and acute pyelonephritis.

The aim of our study was to assess the diagnostic yield of intravenous urography (IVU) compared to ultrasound (US) and computerized tomography (CT) in cases of renal colic, suspected pelvic and abdominal malignancies, suspected renal mass, and acute pyelonephritis. We retrospectively analyzed the case charts of 216 consecutive patients. The patients had been referred to the Department of Radiology by different hospital departments and local general practitioners. All had undergone clinical examination, US and IVU, in that order. When deemed necessary, conventional tomography was performed. Patients with renal masses also underwent CT. In cases without renal colic and normal US examination, the subsequent IVU failed to detect any further important pathology. Hydronephrosis was equally well detected using US and IVU, however, the level of obstruction was better determined using delayed X-ray films. In 24% of cases of renal colics the initial US was normal, however, the IVU revealed ureteric obstruction. Repeat US 8-12 h later always showed hydronephrosis. In 6 of 34 solid renal masses, IVU and conventional tomography failed to make the correct diagnosis, but never could the patient be spared a subsequent CT. IVU is only indicated if US shows hydronephrosis. In cases of renal colic, repeat US is necessary to diagnose the possibly developing hydronephrosis. Clinical history, US and a plain abdominal image will suffice to make the diagnosis. Renal masses always require CT. In these cases, IVU is not necessary. There is no indication left for conventional renal tomographies.

Aortic dissection or renal infarction--multislice computed tomographic angiography can tell.

Acute renal infarction as a consequence of renal artery occlusion often goes unrecognized, mostly due to the non-specific clinical features. A quick diagnosis, ideally within three hours of presentation, is a key to renal function recovery. A 62-year-old male patient was admitted with a sudden abdominal pain, right flank pain and nausea. He had a diastolic hypertension at admission and his previous medical history showed atrial fibrillation. Initial clinical diagnosis was aortic dissection. Laboratory findings included elevated lactate dehydrogenase (LDH) and serum creatinine levels. There were no signs of aortic dissection or aneurismatic lesions registered during a multislice computed tomographic (MSCT) angiography. However, MSCT angiography demonstrated left "upper" renal artery thrombosis and renal infarction--avascular area of the upper two thirds of the left kidney sharply demarcated from the surrounding parenchyma. Both kidneys excreted the contrast. Anticoagulant therapy was initiated, along with antiarrythmic and antihypertensive medications. The follow-up by computed tomography was performed after nine weeks, and it showed a partial revascularization of the previously affected area. Concomitant presence of flank/abdominal pain, an increased risk for thromboembolism and an elevated LDH suggested a possibility of renal infarction. MSCT angiography is a non-invasive and accurate method in the diagnosis of renal artery occlusion and the resulting renal infarction.

The initial investigation in patients presenting with acute flank pain, vomiting, and hematuria is usually a non-contrast CT scan of the abdomen and pelvis to rule out urolithiasis and pyelonephritis, which are the most common reasons for such a clinical presentation. [42] If a non-contrast CT of the abdomen and pelvis is non-contributory, a contrast-enhanced CT of the abdomen should be done to rule out renal infarction as a cause of flank pain. [15] [16] Domanovits et al. suggested that a contrast-enhanced CT should be performed within 24 hours in all patients presenting with the triad of a high risk of thromboembolic events, persistent flank/abdominal/lower back pain, and high LDH levels and/or hematuria. [25]

[Clinical characteristics of patients with acute renal infarction: an analysis of 52 patients in a single center].

To investigate the clinical characteristics of patients with acute renal infarction (ARI) and explore the possible clinical and/or laboratory parameters relative to hematuria. Medical records of 52 patients hospitalized with radiologic proven ARI were retrospectively reviewed. Clinical characteristics, including demographic data, risk factors for thromboembolism, initial clinical presentations, laboratory data, diagnosis, treatment programs and outcomes were evaluated and compared between hematuria(+) and hematuria(-) patients. The mean age of the patients (34 men and 18 women) was (56.3±14.8) years. The left, right, and bilateral kidneys were involved in 44.2%, 34.6% and 21.2% of the patients, respectively. Focal, multiple and massive infarctions were involved in 36.5%, 50.0% and 13.5% of the patients. The prevalence of concurrent thromboembolic events was 38.5%. Atrial fibrillation was complicated in 44.2% of the patients. ARI often presented with nonspecific symptoms, including abdominal/flank pain (71.2%), nausea (55.8%), lumbar pain (53.9%), vomiting (48.1%), fever (48.1%), and diarrhea (21.2%). Percussion tenderness over kidney region was the most common sign (40.4%). The levels of serum lactate dehydrogenase, white blood cell count and C-reactive protein were elevated in 86.5%, 67.3%, and 54.5% of cases, respectively. Hematuria was detected in only 38.5% of the cases on admission. Elevation of serum D-dimer was only noted in 56.5% of the patients. The median duration from hospital presentation to diagnosis was 41.5 h (range: 2-552 h). Contrast-enhanced computed tomography was diagnostic in 47 (90.4%) cases. Angiography was positive in the other 5 (9.6%) cases. Anticoagulation was the most common therapy. During a mean follow-up of (39.4±35.8) months, renal functions of most patients were stable. Four patients needed permanent dialysis and one patient died of heart failure. There was no statistical significance between hematuria (+) group and hematuria (-) group for all the parameters except the level of serum lactate dehydrogenase, which was higher in hematuria(+) group [773.5 IU/L (range: 153.0-3 159.0 IU/L) vs. 488.0 IU/L (range: 137.0-3 370.0 IU/L), P=0.041]. Thromboembolism due to heart disease is the main etiology of ARI. Early contrastenhanced computed tomography scan should be considered for high-risk patients with persisting abdominal or lumbar pain and elevated serum level of lactate dehydrogenase. Hematuria is not a sensitive clue for diagnosis and is not relative to prognosis. Whether it is present may be determined by the severity of infarction.

Case 294: Catastrophic Antiphospholipid Syndrome.

History A 50-year-old woman presented to the emergency department of our hospital with a 2-day history of lower limb pain associated with unusual asthenia and diffuse arthralgia over the past 3 weeks. She was a native of Guinea and had lived in France for most of her life, working as a personal care assistant. Her only medical history of note was an occurrence of fetal death at 12 weeks gestation when she was 35 years old. She had bilateral lower limb swelling, without changes in skin temperature or color. All proximal and distal arterial pulses were felt. General physical examination findings were otherwise unremarkable. Her laboratory tests showed a decreased hemoglobin concentration of 8.9 g/dL (normal range, 12-16 g/dL), a decreased platelet count of 45 × 10<sup9</sup/L (normal range, [150-400] × 10<sup9</sup/L), a C-reactive protein level of 158 mg/L (normal range, <5 mg/L), and a d-dimer level of 2000 mg/L (normal range, <500 mg/L]). Compression US of the lower limbs revealed bilateral calf vein thrombosis involving the fibular and posterior tibial veins. Curative anticoagulation using low-molecular-weight heparin (enoxaparin, subcutaneous injection of 100 units per kilogram of body weight twice a day) was started. The day after the start of anticoagulation therapy, the patient reported dyspnea and acute chest and abdominal pain. Her vital signs were assessed, and she had elevated blood pressure and increased heart rate and respiratory rate, but she remained afebrile. Her cardiac auscultation was unremarkable, besides tachycardia. Skin examination revealed small areas of necrosis on the fingertips of her right hand. Laboratory studies were repeated and showed an increase in serum creatinine level from a baseline value of 0.49 mg/dL to a new value of 1.01 mg/dL (normal range, 0.6-1.1 mg/dL), an apparition of low-grade proteinuria of 0.43 g per day (normal range, <0.3 g/ day), and a high serum troponin level of 1066 ng/L (normal range, <14 ng/L), whereas electrocardiography showed no ST segment modification and echocardiography revealed a moderately altered left ventricular ejection fraction (45%). There was no coronary occlusion seen at emergency coronarography. Contrast-enhanced CT of the chest, abdomen, and pelvis was performed (Figs 1, 2) together with cardiac MRI (Figs 3, 4).

[A case of acute renal failure due to left contracted kidney, complicated by right renal infarction].

A 46-year-old woman, who had been treated with anti-arrhythmic drugs and digitalis for mitral stenosis and paroxysmal atrial fibrillation, suddenly developed severe abdominal pain and nausea. There was tenderness around right CVA. BUN and serum-creatinine were elevated, 57 mg/dl and 4.5 mg/dl respectively. She was in acute renal failure (ARF). WBC, GOT, GPT, LDH were also elevated. Abdominal ultrasonography showed normal-size right kidney (12 cm) and atrophic left kidney (8.5 cm). Selective right renal angiography revealed right renal arterial embolism, suggesting that ARF developed from right renal infarction complicated by left atrophic kidney. Renal scintigram using 99mTc-DTPA indicated non-function type left kidney. Because of the high risk of surgery, she received anticoagulant therapy. Fifteen days later, BUN and serum-creatinine returned to 14mg/dl, 2.2mg/dl, respectively.

End-stage renal disease due to delayed diagnosis of renal tuberculosis: a fatal case report.

Renal TB is difficult to diagnose, because many patients present themselves with lower urinary symptoms which are typical of bacterial cystitis. We report a case of a young woman with renal TB and ESRD. She was admitted with complaints of adynamia, anorexia, fever, weight loss, dysuria and generalized edema for 10 months. At physical examination she was febrile (39 degrees C), and her abdomen had increased volume and was painful at palpation. Laboratorial tests showed serum urea = 220 mg/dL, creatinine = 6.6 mg/dL, hemoglobin = 7.9 g/dL, hematocrit = 24.3%, leukocytes = 33,600/mm(3) and platelets = 664,000/mm(3). Urinalysis showed an acid urine (pH = 5.0), leukocyturia (2+/4+) and mild proteinuria (1+/4+). She was also oliguric (urinary volume < 400 mL/day). Abdominal echography showed thick and contracted bladder walls and heterogeneous liquid collection in the left pelvic region. Two laparotomies were performed, in which abscess in pelvic region was found. Anti-peritoneal tuberculosis treatment with rifampin, isoniazid and pyrazinamide was started. During the follow-up, the urine culture was found to be positive for M. tuberculosis. Six months later the patient had complaints of abdominal pain and dysuria. New laboratorial tests showed serum urea = 187 mg/dL, creatinine = 8.0 mg/dL, potassium = 6.5 mEq/L. Hemodialysis was then started. The CT scan showed signs of chronic nephropathy, dilated calyces and thinning of renal cortex in both kidneys and severe dilation of ureter. The patient developed neurologic symptoms, suggesting tuberculous meningoencephalitis, and died despite of support measures adopted. The patient had ESRD due to secondary uropathy to prolonged tuberculosis of urinary tract that was caused by delayed clinical and laboratorial diagnosis, and probably also due to inadequate antituberculous drugs administration.

Acute Abdomen -- Evaluation

Again, rapid initial diagnosis and treatment of the acute abdomen are crucial. Evaluation and treatment should be simultaneous. Diagnostic interventions include blood work and imaging. In adults older than 40, a 12 lead ECG can help exclude myocardial infarction as the cause of apparent severe abdominal pain. It is important to know if a patient with mesenteric ischemia is in atrial fibrillation. Usually, a complete blood count (CBC), comprehensive metabolic profile and lipase are obtained. For sepsis or mesenteric ischemia, a lactate should be ordered. A urine or serum pregnancy test is needed in the workup of ectopic pregnancy. Diagnostic imaging has advanced rapidly in the past three decades. A bedside ultrasound in the Emergency Department can diagnose cholecystitis, hydronephrosis, hemoperitoneum, and the presence of an abdominal aortic aneurysm in a less than 5 minutes. Diagnostic ultrasound is the preferred modality for cholecystitis, pediatric appendicitis, ruptured ectopic, and ovarian torsion. Multislice helical CT scanning has made the diagnosis of an acute abdomen much more straightforward. In the majority of cases, intravenous (IV) contrast is sufficient. Oral contrast is time-consuming and not usually necessary. MRI is not usually utilized simply because of the time required in a potentially unstable patient. [6] [4] [7]

Case 207: Hodgkin lymphoma with paraneoplastic hypercalcemic pancreatitis.

A 15-year-old girl presented with a 2-month history of 30-lb (13.6 kg) weight loss, chest and abdominal pain, nausea, bilious emesis, cough, and shortness of breath. Initial blood count (performed at an outside hospital) showed elevated white blood cell and platelet counts but low hemoglobin and hematocrit levels. On examination, she had adenopathy in the left axillary and supraclavicular regions, fullness in the left chest, and abdominal guarding. Ultrasonography (US)-guided fine-needle aspiration biopsy of the left anterior chest wall mass was nondiagnostic, and lumbar puncture and bone marrow biopsies were negative. At that time, the patient underwent several imaging studies-including chest radiography; bone scanning; contrast material-enhanced computed tomography (CT) of the chest, abdomen, and pelvis; and fluorine 18 ((18)F) fluorodeoxyglucose (FDG) positron emission tomography (PET)/CT-all performed within 1 week of each other. Pertinent serum laboratory values at the time of these tests were as follows: calcium level, 17 mg/dL (4.25 mmol/L) (normal range, 8.5-10.5 mg/dL [2.1-2.6 mmol/L]); ionized calcium level, 2.3 mmol/L (normal range, 1.1-1.3 mmol/L); lipase level, 2423 U/L (normal level, <300 U/L); amylase level, 1435 U/L (normal level, <140 U/L); lactate dehydrogenase level, 253 U/L (normal level, <240 U/L), albumin level, 2.6 g/dL (26 g/L) (normal level, 3.5-5.0 g/dL [35-50 g/L]), and creatinine level, 1.7 mg/dL (150.3 μmol/L) (normal level, <1.2 mg/dL [<106.1 μmol/L]). A follow-up PET/CT scan was performed approximately 2 months later after initial therapy.

Cases from the Osler Medical Service at Johns Hopkins University.

A 47-year-old white woman with a history of stage III squamous cell carcinoma of the anus was transferred to Johns Hopkins Hospital for further evaluation of renal failure, hemolytic anemia, and thrombocytopenia. The patient was first diagnosed with squamous cell carcinoma of the anus 1 year before admission. She was treated with external beam radiation of the pelvis and two cycles of mitomycin C-based chemotherapy (a cumulative dose, 34 mg/m(2)). Her clinical course was complicated by Clostridium difficile colitis and myositis successfully treated with prednisone. Three months before admission, the patient developed dysuria. Her creatinine increased from normal to 1.7 mg/dL, and microscopic hematuria was present. A renal ultrasound and an abdominal computed tomographic scan showed no abnormalities or obstruction. One month before admission, she underwent a cystoscopy, which showed only radiation-induced changes in the bladder. Two weeks before admission, the patient became delirious and was taken to a hospital, where she was found to be anemic, with a hematocrit level of 23.7%, and thrombocytopenic with a platelet count of 110,000/mm(3). Her creatinine level was 5.9 mg/dL. Previous values of hematocrit, platelet count, and serum creatinine were normal. On admission at Johns Hopkins Hospital the patient had no complaints. She was afebrile on physical examination and had normal vital signs. Head, neck, chest, cardiovascular, and abdominal examinations were normal. There was skin pallor, but no echymoses or petechiae. She was alert and oriented with normal mental status. Her neurologic examination was normal. Laboratory data showed a white blood cell count of 6390/mm(3), a hematocrit level of 26.5%, and a platelet count of 26,000/mm(3). Her blood urea nitrogen level was 57 mg/dL, creatinine level was 4.0 mg/dL, and lactate dehydrogenase was 550 U/L (reference, 115 to 275 U/L). Urinalysis showed innumerable red blood cells and large protein. A peripheral blood smear showed fragmented red blood cells, schistocytes, no abnormal white blood cells, and few platelets. There was no radiographic or clinical evidence of relapse of her squamous cell carcinoma. What is the diagnosis?

Renal infarction in the ED: 10-year experience and review of the literature.

We aimed to describe clinical and radiologic features of acute renal infarction (RI). Clinical, computed tomography (CT), and laboratory findings were retrospectively reviewed for patients diagnosed from 1999 to 2009 with CT proof of acute RI. Possible etiology of infarction was recorded. All available published series of RI were reviewed. Thirty-eight patients with acute RI met inclusion criteria; 127 cases of RI from 7 previous series were pooled for analysis. The most common symptoms were abdominal pain, flank pain, nausea, and vomiting. Leukocytosis (>10 × 10(9)/L) and elevated lactate dehydrogenase levels (>620 IU/L) were the most prominent laboratory findings. Computed tomography features included wedge-shaped hypodensities in the renal parenchyma in 35 (92%) and global renal ischemia in 3 (8%) patients; 13 patients (34%) had concomitant splenic infarction. The most common etiology was atrial fibrillation. Computed tomography determined the specific cause for RI in 5 patients (13%) and a possible etiology in 17 (45%). Exact correlation with previous series was limited by methodological diversity. Renal infarction should be considered in the differential diagnosis of a patient presented to the emergency department with abdominal or flank pain. Laboratory workup should include lactate dehydrogenase levels. After ruling out stone disease, contrast-enhanced CT examination is essential for the diagnosis.

Ischemic colitis

Diagnostic tests There is a recent optical test, but it requires endoscopy (see Diagnosis). There are no specific blood tests for ischemic colitis. The sensitivity of tests among 73 patients were: The white blood cell count was more than 15,000/mm3 in 20 patients (27%) The serum bicarbonate level was less than 24 mmol/L in 26 patients (36%) Plain X-rays are often normal or show non-specific findings. In a series of 73 patients, plain abdominal radiography (56%) showing colic distension in 53% or a pneumoperitoneum in 3%. CT scans are often used in the evaluation of abdominal pain and rectal bleeding, and may suggest the diagnosis of ischemic colitis, pick up complications, or suggest an alternate diagnosis.

[The local lysis therapy of spontaneous renal artery dissection with arterial thrombosis].

A 33-year-old previously completely healthy man developed severe, at first colicky then persisting, pain in the left flank. The blood pressure was 190/110 mm Hg and he had pain over the left kidney on percussion. There was a mild leucocytosis (10,300/microliters), serum creatinine of 1.5 mg/dl and a rise in lactate dehydrogenase level to 395 U/l, while the urine was unremarkable. The pyelogram demonstrated on the left the upper calyceal system only and this very weakly. Colour Doppler ultrasound showed a massively reduced blood flow in the left renal vein while the artery was not visible. Digital subtraction angiography demonstrated eccentric narrowing of the left renal artery by an intravascular thrombus, providing the diagnosis of spontaneous renal artery dissection with thrombosis. Complete recanalization occurred after local thrombolysis with 500,000 IU urokinase over 7 hours, and subsequent administration of four times 40 mg tissue plasminogen activator over 4 hours. But the scintigram still demonstrated impaired renal function with decrease in clearance to 10% of total. The patient was still symptom-free on re-examination 16 months later, serum creatinine concentration was stable at 1.3 mg/dl and the blood pressure was normal.

[Life threatening hypercalcemia in a young man with ALL].

A 16-year-old man experienced fatigue, vomiting and diffuse abdominal pain. Since 4 days he had myalgia in both arms and legs. On examination only a tachycardia of 110/min was noticed. Laboratory tests revealed hemoglobin 12.7 g/dl, leucocytes 10,300/microliter, platelets 89,000/microliter, LDH 191 U/l, sodium 134 mmol/l, potassium 2.76 mmol/l, calcium 4.52 mmol/l (I), creatinine 1.13 mg/dl, urea 72 mg/dl, uric acid 11.2 mg/dl. The levels of PTH (0 pg/ml), PTH-related peptide, vitamin D, vitamin A, IGF-1, STH, 5-HIES and interleukin 6 were within normal limits. TNF-alpha 25.9 pg/ml (< 8.1). The electrocardiography revealed a sinus rythm with a QT-time of 0.28 s (= 100%). Multiple osteolytic bone leasions were seen in thoracic CT-scan. Abdominal sonography showed normal liver structure, multiple subhepatic lymph nodes without splenomegaly. The cytologic examination of the bone marrow demonstrated a diffuse infiltration by a common acute leukemia. The rehydration with physiologic saline (3500 ml/d) was initiated in the ICU. Furosemide was added for further renal excretion. Additionally prednisone (100 mg/d) and calcitonin (300 I.E./d) were given. The calcium level fell within two days. No cardiac arrhythmia nor acute renal failure were seen. After definitive diagnosing the patient was treated corresponding to a specific protocol. One year later the relapsing ALL was diagnosed also by hypercalcemia (5.9 mmol/l). The level of TNF-alpha before and after correction of hypercalcemia was 20 pg/ml. The acute treatment of hypercalcemia is independent of the underlying cause (rehydration with physiologic saline, renal excretion with furosemide, inhibition of osteoclastic activity). The main causes are hyperparathyreoidism or malignancys (90%). We describe TNF-alpha as a possible marker of tumoral load of a common ALL but we are not able to reveal a correlation between TNF-alpha and the calcium level.

[Early and systematic use of ultrasonography in emergency patients with renal colic: analysis of the actual diagnostic efficacy].

In this study, the diagnostic yield of ultrasonography (US) in the early phase of acute urinary obstruction was retrospectively assessed and compared with that of clinical examination. 351 patients were admitted to our emergency department because of suspected renal colic over an 11 months' period: urinary obstruction was subsequently confirmed with other examinations in 76 of them, who were all submitted to renal US within 2 hours of the onset of symptoms. Emergency US results were then retrospectively compared with clinical and laboratory data and the cost of each US exam was calculated. Thirty-nine of 76 patients had negative US findings (51.3%). In the extant 37 patients, US showed hydronephrosis (which was mild in 13 patients and moderate in 6) and renal stones (in 18 patients). Hydronephrosis was associated with renal stones or increased parenchymal echogenicity in 5 and 6 patients, respectively. Pain, which was always severe, was not a useful sign for diagnostic purposes. In contrast, all the 37 patients with abnormal US findings (hydronephrosis, renal stones and increased parenchymal echogenicity) exhibited specific clinical and laboratory abnormalities such as hematuria, ketonuria and marked blood pressure increase (diastolic pressure > 100 mmHg). The same abnormalities, although less severe (mild hematuria and ketonuria and increased diastolic pressure not exceeding 100 mmHg) were nevertheless present in all the 39 patients with negative US findings and yet having a renal colic. The cost of each emergency US exam (calculated on the basis of literature tables and reference cost) was approximately It. L. 104,000. The corresponding total cost for submitting to US all the 76 patients with renal colic was approximately It. L. 7,900,000. In the early phase of urinary obstruction, the association of hematuria, ketonuria and increased blood pressure was more reliable than US findings-the latter method yielding a 51.3% false-negative rate. The presence and severity of the above clinical and laboratory abnormalities might thus represent a criterion to select the patients who are less likely to have positive US findings. This should allow the cost of medical and non-medical staff, equipment and materials to be reduced. As for our personal series, It. L. 28,000,000 was the estimated additional cost of performing US routinely in all the remaining (275) patients with suspected renal colic.

Recurrent renal colic - A case study.

A previously well woman, 44 years of age, presented with 3 years of recurrent bilateral renal colic. Despite an increase in fluid intake and a low calcium diet, the intermittent episodes of renal colic continued and had become more frequent in the last year. An abdominal X-ray was performed, which showed some radio-opaque areas on both renal silhouettes (see Figure 1). Two stones in the right pelvic ureter were also seen following administration of contrast. No obstruction of the urinary tract was evident. Urinalysis revealed leukocyturia, a pH of 6.5 and specific gravity of 1.015. Blood testing showed hypercalcaemia of 2.96 mmol/L and hypophosphataemia of 0.71 mmol/L.

Safety of megadose of vitamin D in patients with nephrolithiasis.

This article describes two patients with renal lithiasis who received a megadose of 25-hydroxy vitamin D (25[OH]D) and had a good outcome. The first case reports a 74-year-old man with a long-term history of renal lithiasis and about four episodes of renal crisis. He was treated once with extracorporeal shock wave lithotripsy. He also had a history of dyslipidemia, myocardial infarction, and stroke. Laboratory tests demonstrated 25(OH)D of 28 ng/mL (normal range (nr): >30 ng/mL), normal lipid levels, creatinine of 1.1 mg/dL, and homocysteine of 26.6 mcmol/L (nr: 5-15 mcmol/L); parathyroid hormone (PTH) was high at 67.3 pg/mL (nr: 10-65 pg/mL), serum total calcium was 8.6 mg/dL, 24-h urinary calcium was 139 mg/d (normal range 100-300 mg/d), and urinary sediment was normal. He received 50 000 IU per week of vitamin D for 3 mo, and 25(OH)D increased to 36.6 ng/mL. Urinary calcium was 142 mg/d, PTH was 46.7 pg/mL, and serum calcium was 9.6 mg/dL. No renal crisis was perceived. He asked for an alternative form of medication since he usually would forget to take drugs. Vitamin D in a single dose of 600 000 IU intramuscular was prescribed. He was asked to increase water intake to 2 to 3 L/d. After 3 mo his 25(OH)D was 75.0 ng/mL, serum calcium was 9.2 mg/dL, urinary calcium was 148 mg/d, and PTH was 38.7 pg/mL. He had no episodes of lithiasis renal crisis. Folic acid and methylcobalamin were added, and homocysteine normalized. At follow-up 3 y later, the patient was asymptomatic, cardiologic evaluation was stable without any other renal lithiasis crises, 25(OH)D continued to be normal at 62 ng/mL, and he received a megadose of vitamin D every 6 mo. Renal ultrasound revealed only microlithiasis. The second case reports a 52-year-old man with a long-term history of renal lithiasis experienced since he was 30 y old, with three renal crisis episodes. He was treated with an extracorporeal shock wave three times. Laboratory tests demonstrated 25(OH)D 18 ng/mL, normal biochemistry, total serum calcium of 10.2 mg/dL, 24-h urinary calcium of 154 mg/d, and normal urinary sediment. He received 50 000 IU per week of 25(OH)D for 3 mo, and 25(OH)D increased to 40.3 ng/mL. Urinary calcium was 167 mg/d, PTH was 35.3 pg/mL, and serum calcium was 10.1 mg/dL. No renal crisis was perceived. He asked for an alternative form of medication, and vitamin D in a single dose of 600 000 IU intramuscular was prescribed. He was asked to increase water intake to 2 to 3 L/d. After 3 mo, his 25(OH)D was 82.0 ng/mL, serum calcium was 9.6 mg/dL, urinary calcium was 175 mg/d, and PTH was 35.3 pg/mL. The renal ultrasound was unchanged. He had no episodes of lithiasis renal crisis. At follow-up 4 y later, the patient was asymptomatic without any other renal lithiasis crises, a renal ultrasound revealed a reduction of calculi size to microlithiasis, 25(OH)D continues normal, and he received a megadose of this vitamin every 4 mo. To the best of our knowledge, this is the first description of a megadose of vitamin D used in patients with nephrolithiasis. Furthermore, this shows the safety of this strategy in patients without hypercalciuria.

The diagnostic yield of intravenous urography: a demographic study.

To examine the impact of intravenous urography (IVU) on patient management in unselected patients in an effort to identify groups in which the use of urography could be reduced. The results of IVU in 235 consecutive unselected patients were assessed prospectively to establish the value of IVU in patient management. Patients were divided into subgroups on the basis of age, sex, presenting symptoms and source of referral. The percentage of examinations with findings affecting patient management was taken as the 'positive diagnostic yield.' Differences between the positive diagnostic yields of IVU in the various groups were examined using the chi 2 test. For all patients the diagnostic yield was 37.4%. In patients over 50 years of age the yield was 46% while below that age the yield fell to 20%. This difference was significant (chi 2 = 13.88, P < 0.001). There were no significant differences between the other defined groups. Specifically, patients referred by general practitioners were as likely to have an IVU abnormality as were patients referred by a hospital practitioner. Patients with painless microscopic haematuria had a lower diagnostic yield (20%) than the other groups examined but this was not significant. IVU has a high diagnostic yield in an unselected population. Although the yield is lower in younger patients IVU offers advantages over other techniques in the investigation of urolithiasis--the commonest positive diagnosis in this study. We argue that it should retain its position as the primary investigation for the majority of patients with urological disease, particularly those suffering loin pain or haematuria.

Acute pancreatitis

At admission age in years > 55 years white blood cell count > 16000 cells/mm3 blood glucose > 11.1 mmol/L (> 200 mg/dL) serum AST > 250 IU/L serum LDH > 350 IU/L At 48 hours Calcium (serum calcium < 2.0 mmol/L (< 8.0 mg/dL) Hematocrit fall >10% Oxygen (hypoxemia PO2 < 60 mmHg) BUN increased by 1.8 or more mmol/L (5 or more mg/dL) after IV fluid hydration Base deficit (negative base excess) > 4 mEq/L Sequestration of fluids > 6 L The criteria for point assignment is that a certain breakpoint be met at any time during that 48 hour period, so that in some situations it can be calculated shortly after admission. It is applicable to both gallstone and alcoholic pancreatitis. Alternatively, pancreatitis can be diagnosed by meeting any of the following:[2] Alternative Ranson score Ranson's score of ≥ 8 Organ failure Substantial pancreatic necrosis (at least 30% glandular necrosis according to contrast-enhanced CT)

[Liver rupture of a subcapsular haematoma after pharmacologic revascularization (Streptokinase) for acute myocardial infarction--case report].

We report the case of a 56 years old male patient, smoker, obese, with untreated arterial hypertension, hospitalized on 16.02.07 with the diagnosis of inferior acute myocardial infarction, for which he received thrombolysis with streptokinase, followed by anticoagulation with non fractioned heparin. Two days later he started to complain of acute abdominal pain, and laboratory findings showed a low hemoglobin level. Imaging findings (ultrasonography and CT scan) showed evidence of subcapsular liver haematoma, caused by bleeding at hepatic and splenic level. He received red blood packed cells, fresh frozen plasma, cryoprecipitate, activated factor VII and was transferred by helicopter to Fundeni Clinical Institute--Intensive care unit (ICU). On admission, the patient was conscious, anxious, dyspneic, with mild hypoxia, with no signs of low cardiac output and with a painful abdomen. ECG, echocardiography and elevated myocardial necrosis enzymes confirmed myocardial infarction. Shortly after admission there was a worsening of his clinical condition, with a decrease in hemoglobin level despite red blood packed cells administration (Hb=7.8 g/dl) and thrombocytopenia (82000/mmc), with normal coagulation tests, thus suggesting active intraabdominal bleeding. Echography and CT scan confirmed bleeding. Emergency surgery was performed, showing massive haemoperitoneum (approx 4.5 L of blood), due to spontaneous rupture of a subcapsular hematoma in the liver. The surgical hemostasis was performed on the liver parenchyma laceration. Duration of surgery was 4 hours. There were no significant cardiac events during surgery (no signs of ischemia on ECG, no ST elevation), despite the need for inotropic agent. After surgery, the patient was referred to the ICU, intubated and ventilated, with inotropic support - dobutamine. Sequential ECG's, enzymatic trend and echocardiographies were performed to monitor myocardial ischemia. The outcome was favourable, no further bleeding and no postoperative myocardial infarction occurred. Secondary prevention was started early (thromboprophylaxis, selective beta-blocker, angiotensin inhibitors and statins). The patient had a favorable outcome and was discharged from the ICU the fourth day after surgery. He had a total length of stay in hospital of seven days, with a follow-up in the cardiology department.

The only findings of renal infarction in a non-contrast CT abdomen may be some perinephric stranding and mild renal swelling, but these can easily be misinterpreted as signs of a recently passed kidney stone. The standard test for a suspected renal infarction is a contrast-enhanced CT scan of the abdomen which should be done in cases of possible renal infarction with negative non-contrast studies, especially in patients with elevated LDH, atrial fibrillation, increased risk, or history of thrombosis, or elevated age (>70).

Resolution of proteinuria secondary to bilateral renal vein thrombosis after treatment with systemic thrombolytic therapy.

A case of significant proteinuria occurred as a result of bilateral renal vein thrombosis secondary to dehydration, which resolved after treatment with urokinase. The patient developed nausea and vomiting from viral gastroenteritis with subsequent volume contraction. He later noted the onset of aching lower abdominal and flank pain. On admission, he was noted to have a serum creatinine of 1.7 mg/dL, and 4+ proteinuria on urinalysis. A 24-hour urine collection showed 2.34 g protein. A renal venogram showed bilateral renal vein thrombosis (RVT) without involvement of the inferior vena cava. Therapy was initiated with heparin at 1,000 U/hr, followed by intravenous (IV) urokinase, 4,400 U/kg bolus, followed by 4,400 U/kg/hr with continuous infusion for 12 hours. A repeat renal venogram done at this time showed partial resolution of thrombosis bilaterally. A second 12-hour infusion of urokinase at 5,000 U/kg/hr was performed; at this time, the patient reported resolution of his flank and abdominal pain. A repeat 24-hour urine collection showed 60 mg protein with a normal creatinine clearance. Levels of antithrombin III, protein C, and protein S were all normal. A renal biopsy was performed and showed normal histology on light, immunofluorescent, and electron microscopic evaluation. The patient has done well on no therapy and has had no recurrence of thrombosis or proteinuria after 2.5 years. This is a US government work. There are no restrictions on its use.

[Acute renal failure as atypical complication of atrial fibrillation].

We present a case of a 76-year-old woman with persistent atrial fibrillation, recent diagnosis of ischemic stroke and embolic occlusion of the iliac artery, who was admitted to our department with symptoms of acute renal failure. Using the data from medical history, physical examination, ECG, laboratory tests (urinalysis, LDH in serum and urine) and radiologic studies (color Doppler ultrasound, angio-CT) we diagnosed renal artery embolus and infarct of solitary functioning kidney. We presumed that this complication was related to the inadequate anticoagulation in the course of atrial fibrillation. Patient received intravenous heparin followed by oral warfarin and started renal replacement therapy.

[Right-sided prosthetic cardiac valve thrombosis: value of cinefluoroscopy in the diagnosis and follow-up of thrombolytic treatment].

A 33-year-old woman (Pt. A) with a prosthetic cardiac valve in the pulmonary position [CarboMedics bileaflet valve, diameter 23 mm] as part of the repair of a tetralogy of Fallot 4 years previously, and a 51-year-old woman (Pt. B) with a prosthetic cardiac valve [St. Jude Medical bileaflet valve, diameter 31 mm] inserted in tricuspid position as replacement of a degenerated Hancock bioprosthetic valve inserted 15 years previously, 10 years after an episode of endocarditis, were admitted to hospital with dyspnea and chest pain and dyspnea and tachycardia, respectively. Pt. A had a 3 - 4/6 crescendo-decrescendo systolic murmur and a 2/6 early diastolic decrescendo murmur over the 2nd to 4th right intercostal space (ICS), while Pt. B had a 3/6 holosystolic murmur and a 2 - 3/6 diastolic murmur over the 4th right ICS. Closing click was missing in both patients. Blood tests demonstrated an elevated LDH (404 U/l) in Pt. A and an elevated GGT (108 U/l) and fibrinogen (449 mg/dl) in Pt. B. Anticoagulation was below the therapeutic level, with an INR value of 1,65 and 1,93, respectively. The electrocardiogram showed sinus rhythm, right bundle branch block and an isoelectric ST-segment (Pt. A) and a typical high-frequency atrial flutter with a 2:1 block, right bundle branch block and terminal T-wave inversions in leads V1 to V5 (Pt. B). Cinefluoroscopy showed rigid and hypomobile leaflets as a result of prosthetic cardiac valve thrombosis. Doppler echocardiography confirmed the stenosis of the prosthetic valve in the pulmonary position (peak gradient 73 mm Hg, mean gradient 34 mm Hg) and the tricuspid position (mean gradient 8.48 mm Hg, peak gradient 16.73 mm Hg). Both patients were treated with unfractionated heparin and urokinase single-bolus injection of 4400 U/kg over 10 min followed by an infusion of 4400 U/kg/h over 12 h. Both patients had an abnormal opening angle, which improved to a normal opening and closing angle. Doppler echocardiography demonstrated decreased peak (18.0 and 6.6 mm Hg, respectively) and median gradients (9.0 and 2.6 mm Hg, respectively). No further complications (such as bleeding, embolism, delayed surgical treatment, rethrombosis) had occurred, and both patients became asymptomatic. After oral anticoagulation in a therapeutic INR range for 12 and 4 months, respectively, prosthetic heart valve function continued to be normal in both patients. Thrombolysis appears to be an efficacious and safe treatment in patients with thrombosis of a prosthetic cardiac valve in the pulmonary or tricuspid position, and it may be used as first-line therapy. Cinefluoroscopy is a simple and accurate method both in the diagnosis of prosthetic cardiac valve thrombosis and in following the response to thrombolytic treatment.