Abstract
A previously healthy, 35-year-old woman, mother of two children, presented with a 3-day history of abdominal discomfort, vomiting and anuria for 2 days. She had no history of diabetes or hypertension. She had been using a combination of ethinylestradiol and drospirenone as a contraceptive for the previous 3 years. Her investigations at presentation were: serum creatinine: 7.9 mg/dL (698 μmol/L), blood urea nitrogen: 185 mg/dL (66 mmol/L), serum proteins: 8.2 g/dL, serum albumin: 4.5 g/dL, serum homocysteine: 4.2 μmol/L (0.56 mg/L), haemoglobin: 11.2 g/dL, total leucocyte count: 4800/mm3, platelet count: 340 × 109/L, prothrombin time: 15.0 sec (control: 13.0 sec), activated partial thromboplastin time: 28.0 sec (control: 30.0 sec), thrombin time: 10.0 sec (control: 8.0 sec), bleeding time: 4.0 min (reference range: 2.0–7.0 min), clotting time: 5.0 min (reference range: 5.0–7.0 min), serum fibrinogen: 444 mg/dL (range: 150–400 mg/dL) and D-dimer: 1.7 μg/mL (range: 0.5 μg/mL). Kidney sizes on ultrasound were right: 12.4 × 4.6 cm and left: 11.5 × 4.4 cm. Doppler of the renal arteries revealed severe decrease and pruning of the segmental, inter-lobar and arcuate vessels and absence of the cortical blush in both of the kidneys. Urine dipstick examination for proteins was negative. A renal biopsy was done after a session of haemodialysis. It revealed coagulative necrosis (infarct) of the cortex of the kidney, and the artery included in the biopsy was obstructed by fibrin thrombus (Figure 1). She was not pregnant and had no congenital heart disease. There was no history of acute gastroenteritis, trauma or snakebite. There was no history or clinical features suggestive of haemolytic uraemic syndrome. There were no schistocytes on peripheral smear. Electrocardiogram showed normal sinus rhythm with no ischaemic or chamber enlargement changes. Echocardiography revealed normal cardiac chambers and normal valves. The reports of anti-thrombin III: 0.25 g/L (range: 0.19–0.31 g/L), protein C: 90% (range: 70–160%) and protein S: 80% (range: 60–150%). Prothrombin time and partial thromboplastin times were not prolonged in order to investigate for factor V Leiden mutation. Flow cytometry did not find a reduction in CD 55 and CD 59 on red blood cells, thus excluding paroxysmal nocturnal haemoglobinuria. Anti-phospholipid antibodies, lupus antibody, anti-nuclear antibodies and anti-double-stranded DNA were negative. Fig. 1. Renal biopsy showing cortical necrosis and the artery occluded by fresh fibrin thrombus (arrow) in an artery (SMPASX40). The patient did not regain renal function. She was initiated on continuous ambulatory peritoneal dialysis. One of the adverse effects of oral contraceptive pills is arterial thrombosis. There are experimental reports of acute cortical necrosis in rats induced by oestrone and vasopressin administration [1]. There are a few reports of acute cortical necrosis in patients who used oral contraceptives, but these patients had other features like factor V Leiden mutation [2] and smoking [3].
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