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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 {genzyme}

A male nephrotic patient with rapid decline of renal function

Douglas A. Charney1, Ashutosh Singh2 and Narcis Aron2

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

The first 10% of the full text of this article appears below.



   Case
 
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 . . . [Full Text of this Article]



   Discussion
 


   Teaching points
 

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