A 16-year-old nephrotic patient with chest pain.

A 10-year-old boy who had been born in Pakistan, but had lived in England since the age of 9, initially presented to a paediatric hospital with nephrotic syndrome. He responded promptly to corticosteroids and was followed in outpatients. For 4 years he had several relapses of his nephrotic syndrome, which were successfully treated with courses of corticosteroids. After he had been abroad without medical review for 1 year, he returned aged 15 with nephrotic range proteinuria that persisted despite taking corticosteroids and levamisole. At the age of 16 his care was transferred to an adult nephrology unit where he was assessed in the outpatient clinic. He appeared cushingoid and the blood pressure was 120/70mmHg. The serum creatinine was 68mmol/l, the serum cholesterol 15.7mmol/l, the serum albumin 28 g/l and the urinary protein excretion 5.8 g/day. Only a few days after his first assessment at the adult nephrology unit he was admitted to hospital with gripping central chest pain. There was no history of smoking, diabetes mellitus or premature cardiac disease in his family. Physical examination was unremarkable. Figure 1 shows his electrocardiogram. The admitting doctor suspected pericarditis as a cause of his chest pain. Later review of his laboratory results (creatine kinase 1067 IU/l, aspartate aminotransferase 105 IU/l) accompanied by continued chest pain prompted urgent coronary angiography (Figure 2). This showed partial thrombotic occlusion of the left main stem and complete occlusion of the left anterior descending artery (LAD). He was treated with aspirin, thrombolysis and heparin. One day later, repeat coronary angiography showed persistent occlusion of the LAD. Thrombectomy and stent insertion were performed (Figure 3). The patient made a good recovery and was discharged taking aspirin, clopidogrel, atorvastatin, metoprolol and warfarin. A kidney biopsy several months later confirmed minimal change nephropathy (Figure 4). He received a 12 week course of cyclophosphamide and has remained in remission since (3 years). His serum cholesterol normalized following remission of the nephrotic syndrome. A familial cause for hypercholesterolaemia was ruled out after testing his parents and two siblings.