Abstract: TH-PO0835
From Bulk to Burden and Back to Balance: Uncovering Anabolic Steroids as a Reversible Cause of Proteinuria
Session Information
- Glomerular Case Reports: Potpourri
November 06, 2025 | Location: Exhibit Hall, Convention Center
Abstract Time: 10:00 AM - 12:00 PM
Category: Glomerular Diseases
- 1402 Glomerular Diseases: Clinical, Outcomes, and Therapeutics
Authors
- Pascoal, Felipe, Centro Brasiliense de Nefrologia Ltda, Brasília, DF, Brazil
- Pascoal, Pedro Guimaraes, Centro Brasiliense de Nefrologia Ltda, Brasília, DF, Brazil
- Xavier, Kelia, Centro Brasiliense de Nefrologia Ltda, Brasília, DF, Brazil
- Simon, Adolfo, Centro Brasiliense de Nefrologia Ltda, Brasília, DF, Brazil
- Bello, Vilber, Centro Brasiliense de Nefrologia Ltda, Brasília, DF, Brazil
- Lauar, Juliane, Centro Brasiliense de Nefrologia Ltda, Brasília, DF, Brazil
- Pascoal, Istenio, Centro Brasiliense de Nefrologia Ltda, Brasília, DF, Brazil
Introduction
Anabolic-androgenic steroids (AAS) are testosterone derivatives increasingly misused for aesthetic purposes by young and middle-aged adults, with up to 4 million users in the U.S alone. Although cardiovascular and endocrine risks are recognized, renal effects remain underappreciated. AAS-related glomerular damage involves oxidative, hormonal, and immune mechanisms. This case highlights a rare but potentially reversible form of near-nephrotic proteinuria associated with AAS use, stressing the value of early suspicion and swift intervention in comparable scenarios.
Case Description
A 55-year-old man with well-controlled HIV was referred for evaluation of asymptomatic proteinuria. He reported continuous use of injectable testosterone and nandrolone over the prior 12 months, before which urinalysis showed no proteinuria. At presentation, exams showed proteinuria of 3.3 g/24h and albuminuria of 1.7 g/24h. Combined creatinine-cystatin C eGFR was 83 mL/min/1.73m2; physical exam was unremarkable and urinary sediment was inactive. Chronic medications (rosuvastatin, isotretinoin, multivitamins) were unchanged. Given Blood Pressure at 102/68 mmHg and serum potassium levels between 5.2–5.4 mEq/L, RAAS inhibitors were withheld. AAS were discontinued, and, after one month, proteinuria dropped to 0.3 g/24h and albuminuria to 0.04 g/24h (Figure 1). Bioimpedance showed stable and unchanged lean mass and weight (209 lbs) during follow-up and renal function remained stable, obviating the need for biopsy.
Discussion
This case highlights the rare, often-overlooked nephrotoxicity of AAS and the need to consider them in the differential diagnosis of new-onset proteinuria when plausible. The close temporal relationship between drug suspension and marked remission of proteinuria offers compelling support for a direct causal link. Timely recognition and withdrawal of AAS can restore renal integrity while sparing patients from invasive procedures and progressive harm.