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Development of Focal Segmental Glomerulosclerosis after Anabolic Steroid Abuse

Leal C. Herlitz^*, Glen S. Markowitz^*, Alton B. Farris, Joshua A. Schwimmer^,, Michael B. Stokes^*, Cheryl Kunis, Robert B. Colvin and Vivette D. D'Agati^*

Departments of *Pathology and
Medicine, Columbia University, College of Physicians and Surgeons, New York, New York;
Department of Medicine, Lenox Hill Hospital, New York, New York; and
Department of Pathology, Massachusetts General Hospital, Harvard Medical School, Boston, Massachusetts

Correspondence: Dr. Vivette D. D'Agati, Columbia University College of Physicians and Surgeons, Department of Pathology, VC14-224, 630 West 168th Street, New York, NY 10032. Phone: 212-305-7460; Fax: 212-342-5380; E-mail: vdd1{at}columbia.edu

Received for publication April 28, 2009. Accepted for publication September 17, 2009.

Anabolic steroid abuse adversely affects the endocrine system, blood lipids, and the liver, but renal injury has not been described. We identified an association of focal segmental glomerulosclerosis (FSGS) and proteinuria in a cohort of 10 bodybuilders (six white and four Hispanic; mean body mass index 34.7) after long-term abuse of anabolic steroids. The clinical presentation included proteinuria (mean 10.1 g/d; range 1.3 to 26.3 g/d) and renal insufficiency (mean serum creatinine 3.0 mg/dl; range 1.3 to 7.8 mg/dl); three (30%) patients presented with nephrotic syndrome. Renal biopsy revealed FSGS in nine patients, four of whom also had glomerulomegaly, and glomerulomegaly alone in one patient. Three biopsies revealed collapsing lesions of FSGS, four had perihilar lesions, and seven showed 40% tubular atrophy and interstitial fibrosis. Among eight patients with mean follow-up of 2.2 yr, one progressed to ESRD, the other seven received renin-angiotensin system blockade, and one also received corticosteroids. All seven patients discontinued anabolic steroids, leading to weight loss, stabilization or improvement in serum creatinine, and a reduction in proteinuria. One patient resumed anabolic steroid abuse and suffered relapse of proteinuria and renal insufficiency. We hypothesize that secondary FSGS results from a combination of postadaptive glomerular changes driven by increased lean body mass and potential direct nephrotoxic effects of anabolic steroids. Because of the expected rise in serum creatinine as a result of increased muscle mass in bodybuilders, this complication is likely underrecognized.

Copyright © 2009 by the American Society of Nephrology. Online ISSN: 1533-3450 Print ISSN: 1046-6673