NDT Advance Access originally published online on February 16, 2005
Nephrology Dialysis Transplantation 2005 20(6):1263-1266; doi:10.1093/ndt/gfh724
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© The Author [2005]. Published by Oxford University Press on behalf of ERA-EDTA. All rights reserved. For Permissions, please email: journals.permissions@oupjournals.org
Teaching Point
(Section Editor: Alain Meyrier)
Supported by an educational grant from
A male nephrotic patient with rapid decline of renal function
1 Department of Pathology and 2 Department of Internal Medicine, Nephrology Division, St Luke's-Roosevelt Hospital Center, New York, NY, USA
Correspondence and offprint requests to: Douglas A. Charney, MD, St Luke's Hospital, Department of Pathology, Clark 4, 1111 Amsterdam Avenue, New York, NY 10025, USA. Email: dcharney@chpnet.org
Keywords: crescent; fibrin crescent; membranous nephropathy
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A 56-year-old African American male presented to the emergency room after 2 weeks of gradually worsening dyspnoea, cough, periorbital and lower extremity oedema, a 20 lb weight gain and dark coloured urine. The patient had a history of hypertension and hypercholesterolaemia, and had been treated with hydrochlorothiazide, lisinopril and atorvastatin.
Three months previously, his blood urea nitrogen (BUN) was 22 mg/dl (7.8 mmol/l), serum creatinine was 1.3 mg/dl (115 µmol/l) and urinalysis showed 3+ proteinuria by dipstick.
Currently, his physical examination revealed a blood pressure of 177/125 mmHg and periorbital and 3+ lower extremity oedema. Initial abnormal laboratory data included BUN of 47 mg/dl, serum creatinine of 3.5 mg/dl, albumin of 1.2 gm/dl, cholesterol of 348 mg/dl, triglycerides of 252 mg/dl and serum creatine kinase of 783 U/l. Blood cell counts
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