Cerebral infarction in patient with minimal change nephrotic syndrome
A 68-year-old retired office manager (male) was admitted to the hospital with worsening epigastric pain, clay colored stools, nausea, and ankle swelling. He also complained of weakness and tingling in left arm, slurred speech and difficulty getting words out. His risk factor for cerebro-vascular disease included only hypertension that was well-controlled with felodipine. On examination, there was non-pitting pedal edema, right-sided cerebellar signs (past pointing, dysdiadochokinesia), left hemiparesis, and expressive dysphasia. Blood pressure was 180/90 mmHg. Urine Dipstick had 2+ blood, 4+ protein with urinary Protein creatinine ratio of 1401 (approx. 14 g/day). Renal function was mildly impaired with creatinine at 168 μmol/L. Albumin was low at 16 g/L. Cholesterol was elevated at 13.8 mmol/L.\nComputed tomography (CT) and magnetic resonance imaging (MRI) of the brain showed widespread cerebral infarcts in the middle cerebral and posterior cerebral artery territory [Figures and ]. Transthoracic echocardiogram and carotid doppler did not show any abnormality. Renal biopsy showed minimal change disease [Figures –]. Auto immune profile and compliments were normal. Immunoelectrophoresis did not show any plasma cell dyscrasia. Protein C and S levels were at lower end of normal range that was considered secondary to renal loss rather than primary deficiency.\nOther investigations for hypercoagulable state such as anti-cardiolipin antibodies, factor V leiden mutation were within normal limits.\nContrast CT of chest/abdomen/pelvis looking for malignancy was within normal limits.\nInfarcts were considered secondary to arterial thombosis as a result of hypercoagulable state seen in nephrotic syndrome. Patient was treated with antiplatelet agents like aspirin and clopidogrel. Patient did not receive any prophylactic or therapeutic anticoagulation with heparin or low molecular weight heparin during his hospital stay. Nephrotic syndrome was treated with three doses of intravenous methyl prednisone and was started on oral prednisone at 1 mg/kg that was tapered down over a period of 3 months. There was good response to treatment with resolution of proteinuria and improvement in renal function. Most recent albumin has come up to 36 g/L. Patient remains in remission till date and has not had any further thrombotic episode.