ADVANCED KIDNEY AND HEART FAILURE IN A VERY FIT MAN – WHAT’S THE CASE?

R HONG1, A PRASHAR2, J SAAB4, B GRAY2, I KATZ1,3

1Department of Renal Medicine, St George Hospital, Kogarah, Australia, 2Department of Cardiology, St George Hospital, Kogarah, Australia, 3UNSW St George Clinical School, Kogarah, Australia, 4Department of Anatomical Histopathology, St George Hospital, Kogarah, Australia

Background: Several sport supplements used to enhance muscle strength, performance and weight loss are implicated in organ damage. Aristocholic acid (AA) in weight-loss pills is the causal nephrotoxin in rapidly-progressive Chinese herbal nephropathy. Illegal supplements like anabolic steroids (AS) are associated with significant cardiovascular morbidity causing hypertension, left ventricular (LV) hypertrophy, infarction, myocarditis and CKD.
Case Report: A fit 52-year-old law-enforcement officer presented with three-week history of haemoptysis, orthopnoea and peripheral oedema following rhinovirus infection. Echocardiogram revealed severe dilated cardiomyopathy (CMO) later complicated by LV thrombus. He had advanced renal impairment (creatinine 229µmol/L, eGFR 27ml/min/1.73m2), nephrotic syndrome (proteinuria 11g/24hr, hypoalbuminemia 21g/L) and hypertension. His only medical background was polycythaemia, diet-controlled dyslipidaemia and provoked DVT. He exercised regularly including heavy weightlifting and used extensive nutritional supplements. On further questioning he admitted DHEA and AA use to enhance combat performance but denied AS use. Glomerulonephritis screen for infectious/autoimmune/malignant/infiltrative disease was negative. Renal biopsy showed advanced focal segmental glomerulosclerosis, severe interstitial fibrosis, tubular atrophy and arteriosclerosis without acute inflammatory infiltrates or granulomas. Immunofluorescence and electron microscopy were unremarkable. Cardiac MRI confirmed dilated CMO without infiltrative disease, global systolic dysfunction (LVEF 26%), increased LV mass suggesting severe hypertension, ischaemic subendocardial-fibrosis with LAD disease on angiogram, and non-ischaemic midwall-fibrosis with elevated CK7000U/L suggesting myocarditis. PET/CT opposed sarcoidosis. Management included diuresis, beta-blockers and steroid trial with some functional improvement; LVEF 30%, creatinine 167umol/L, eGFR 40ml/min/1.73m2.
Conclusions: This case reflects acutely decompensated CMO and renal failure with recent viral infection, on background of chronic kidney and heart disease. Aetiology remains unclear. AA-nephropathy explains interstitial fibrosis but not glomerulosclerosis. DHEA (AS precursor) or unconfessed AS use could explain both cardiac and renal pathology.


Biography:
Regina is a Basic Physician Trainee at St George Hospital with a passion for renal medicine and palliative care. Research interests include progression and complications of chronic kidney disease, renal supportive care as well as health policy, planning and management.

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