Anuria suggests complete urinary tract obstruction, acute cortical necrosis, or massive vascular occlusion. We report a case of bilateral renal artery thrombosis in an 87-year-old woman who presented to the emergency department with abdominal pain, diarrhea, and anuria within the past 24 hours. Serum creatinine on admission was 5.87 mg/dl and urea was 100 mg/dl. Computed tomography showed renal artery thrombosis and partial splenic infarction. A conservative approach was performed with anticoagulation with warfarin. The patient recovered months later from renal function and urinary output.
introduction
Anuria may indicate complete urinary tract obstruction, acute cortical necrosis, or massive vascular occlusion. Renal infarction is rare (prevalence estimated at 14 per 1000 from autopsy studies [1]) and underdiagnosed because the symptoms are mostly non-specific at the time of presentation. The two main causes of renal infarction are thromboembolism and thrombosis in situ; Embolus usually arises from a thrombus in the heart or aorta, and thrombosis in situ usually results from an underlying condition of hypercoagulability or injury or dissection of a renal artery. Renal infarction occurs more frequently in patients with atrial fibrillation, cardiomyopathies and/or valvular heart disease [2].
The authors report a case of renal infarction caused by bilateral renal artery embolism in a patient with paroxysmal atrial fibrillation and hypertrophic cardiomyopathy.
case presentation
We present the case of an 87-year-old woman with a history of hypertrophic cardiomyopathy, mild aortic stenosis, paroxysmal atrial fibrillation, and hypertension on perindopril, indapamide, lercanidipine, and nebivolol. She was admitted to the emergency room for abdominal pain, diarrhea and anuria in the past 24 hours. Six days earlier she had been prescribed amoxicillin/clavulanic acid and ibuprofen for a respiratory infection and three days earlier she had been treated for focal momentary neurological deficits, presumably due to a transient ischemic attack (TIA). On examination her blood pressure was 170/80 mmHg and she complained of discomfort on abdominal palpation. Laboratory tests revealed acute kidney injury (serum creatinine: 5.87 mg/dL; urea: 100 mg/dL) and elevated C-reactive protein (218 mg/L) and lactate dehydrogenase (LDH) (679 U/L). Urine could not be collected because of anuria. Kidney ultrasound showed normal kidneys without hydronephrosis. The electrocardiogram showed a sinus rhythm. Despite endovascular fluids, the patient remained anuric, became hypervolemic, and required hemodialysis. A CT scan was performed to rule out vascular events and revealed bilateral renal artery thrombosis and partial splenic infarction (Fig 1–4). The echocardiogram (transthoracic and transesophageal) showed a 25 mm inferior vena cava (without respiratory variability), predominant apical distribution of hypertrophic cardiomyopathy, and this was considered a possible cause of the thromboembolism, although no vegetation or thrombi were seen. Antiphospholipid syndrome was excluded (titres of anti-beta-2-glycoprotein, anticardiolipin antibodies and lupus anticoagulant activity were negative at baseline and at three months). Endovascular treatment was dispensed with due to uncertain time since the infarction, and anticoagulation was started first with low molecular weight heparin and then with warfarin (choice considered adequate since the patient was on dialysis). One month later the patient developed diuresis, two months later she was off dialysis and currently has a serum creatinine of 1.3 mg/dL.
discussion
Renal infarction should be strongly considered when the following triad is present: persistent abdominal and/or flank pain, elevated serum LDH and/or hematuria, and risk of a thromboembolic event [3].
The occurrence of bilateral renal artery embolization resulting in acute renal failure is extremely rare, with most cases being due to cardioembolism, particularly in patients with atrial fibrillation, cardiomyopathies, or valvular heart disease [3,4].
Given the rarity of this disease, there is insufficient evidence on therapeutic options. Thrombolytic therapy is typically reserved for patients with early disease diagnosis, with the optimal time from port to treatment being 90 to 180 minutes [5,6]. In the presented case, endovascular treatment was dispensed with due to a late diagnosis (>24 hours after the onset of symptoms) and anticoagulation was started. A thromboembolism secondary to atrial fibrillation was considered to be the cause of the bilateral embolism of the renal arteries. The patient had a favorable clinical development with only anticoagulation and had an almost complete recovery of renal function.
Conclusions
In this case of acute kidney injury, the previous diagnosis of paroxysmal atrial fibrillation, the presence of anuria, elevated serum LDH, history of TIA, and splenic infarction were important diagnostic clues, which were later confirmed by contrast-enhanced CT.
Despite persistent anuria and apparent dysfunction of the renal arteries, which is why endovascular therapy was dispensed with, the patient had a very favorable clinical course with complete restoration of renal function.
Nevertheless, the authors emphasize the need for early diagnosis to reduce the risk of progression to chronification and to improve prognosis.
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