Abstract
Background:
IgA nephropathy (IgAN) is the most common primary glomerulonephritis and typically presents with hematuria following mucosal infection. Adult-onset cutaneous leukocytoclastic vasculitis (LCV) as the initial manifestation of IgAN is uncommon and may delay recognition of underlying renal involvement. Anabolic-androgenic steroids (AAS), classified as Schedule III controlled substances under federal law, remain widely accessible through non-prescribed channels despite regulatory oversight. Emerging evidence suggests AAS may alter immune regulation, endothelial integrity, and cytokine signaling, potentially contributing to secondary glomerular injury.
Case Presentation:
A 24-year-old male presented with progressive necrotic pretibial plaques evolving from pruritic erythematous papules. His history was notable for performance-enhancing hormone use, including testosterone, growth hormone, and nandrolone decanoate. Skin biopsy demonstrated acute leukocytoclastic vasculitis with fibrinoid necrosis with a negative direct immunofluorescence. Subsequent evaluation identified nephrotic-range proteinuria (ACR 3,265 mg/g), elevated cystatin C, and reduced estimated glomerular filtration rate (eGFR ~76 mL/min/1.73 m²). Renal biopsy confirmed IgA nephropathy with mesangial immune complex deposition.
Discussion:
The patient was treated with corticosteroids, renoprotective therapy, and a nine-month course of targeted-release budesonide. Follow-up demonstrated an 85% reduction in urinary albumin, a 73% decrease in ACR, and improved eGFR to 102 mL/min/1.73 m². Cutaneous lesions resolved without recurrence. This case illustrates an atypical extra-renal presentation of IgA nephropathy and raises concern that anabolic hormone exposure may serve as a potential immune-modulating trigger. It also highlights a broader policy gap: current steroid regulation prioritizes criminal control over preventive education and medical risk awareness. Early clinician screening and public health education regarding anabolic steroid–associated systemic complications may help mitigate preventable renal morbidity.
