Abstract: FR-PO0720
Beyond Anabolic Steroids: FSGS Associated with Testosterone Replacement Therapy
Session Information
- Glomerular Diseases: Membranous Nephropathy, FSGS, and Podocytopathies
October 23, 2026 | Location: Exhibit Hall A, Convention Center
Abstract Time: 10:00 AM - 12:00 PM
Category: Glomerular Diseases
- 1402 Glomerular Diseases: Clinical, Outcomes, and Therapeutics
Authors
- Memar, Shadi, Pennsylvania Hospital, Philadelphia, Pennsylvania, United States
- Sabbouh, Toni, Pennsylvania Hospital, Philadelphia, Pennsylvania, United States
Introduction
Focal segmental glomerulosclerosis (FSGS) represents a histologic pattern of glomerular injury with many etiologies. Secondary FSGS can result from physiologic responses to obesity, hypertension, viral infections, medications, and increasingly recognized, anabolic steroid or testosterone use. We present a case of biopsy-proven FSGS in an elderly man on testosterone supplementation for hypogonadism, with significant proteinuria improvement following testosterone discontinuation.
Case Description
An 80-year-old male with a past medical history of hypertension, atrial fibrillation, and hypogonadism on testosterone for 10 years was referred to nephrology for evaluation of progressive proteinuria with preserved renal function. Workup was negative for hepatitis, HIV, monoclonal gammopathy, complement abnormalities, ANA, and anti-PLA2R antibody. He was maintained on irbesartan and spironolactone. Kidney biopsy revealed FSGS (NOS variant). Given the secondary nature of his FSGS and the lack of other identifiable secondary causes, the patient’s testosterone was discontinued, and empagliflozin was initiated for additional proteinuric benefit. The patient demonstrated marked improvement in proteinuria, with urine albumin creatinine ratio (UACR) decreasing by 70% in 10 months (Figure 1). Renal function remained stable with an eGFR in the 70s. At his most recent follow-up, he remained clinically stable on conservative medical management.
Discussion
While anabolic steroid-associated FSGS has been well-described, testosterone replacement therapy at therapeutic doses represents an underrecognized cause of FSGS. The temporal relationship between testosterone use and progressive proteinuria, combined with marked improvement after cessation, strongly suggests a causal relationship. Conservative management with optimization of RAAS blockade and SGLT2 inhibition proved effective, avoiding the need for immunosuppression. This case highlights the importance of medication review in evaluating secondary causes of FSGS and supports testosterone as a reversible cause of podocyte injury.