The Lancet
Yvo Smulders, Cees-Jan Oostwouder, Frank Stam
In August, 2003, a 39-year-old anesthestist went for a routine physical examination. He had minor non-specific abdominal complaints, which subsided spontaneously and he decided it would be a good idea to have a check-up. His medical history was unremarkable, apart from a congenital single kidney. He had noticed increased hair loss during the previous year. His family history was positive for hypercholesterolaemia (his mother had a total cholesterol of >8·0 mmol/L). Physical examination showed alopecia (figure 1, A) and hypertension (160/ 105 mm Hg), but no other abnormalities. Further tests were done which showed renal insufficiency (serum creatinine 160 mmol/L; urinary creatinine clearance 66 mL/min), and hypercholesterolaemia (total cholesterol 9·6 mmol/L; LDL cholesterol 7·2 mmol/L). Urine analysis showed no proteinuria and a normal urinary sediment. An electrocardiogram showed ST-segment elevation in the anteroseptal leads and negative T waves in the anterolateral leads (figure 2, A). The same day, he was seen by a cardiologist, who ordered tests for cardiac enzymes. Although total serum creatine phosphokinase was elevated (744 U/L), the creatine phosphokinase-MB isoenzyme fraction and troponin-T concentrations were within normal limits. He was then given the diagnoses of hypertension, familial hypercholesterolaemia, hypertensive renal disease of his single kidney, and chronic symptomless ischaemic heart disease. He was referred to our outpatient clinic for treatment, where he arrived in quite a bad mood.
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