Abstract: TH-PO0871
AKI in an HIV-Positive Patient Following Amphetamine Use: A Biopsy-Proven Case of Immune Complex Glomerulonephritis and Acute Interstitial Nephritis
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
- Liwanag, Genecarlo, SLMC, Saint Luke's Medical Center - Global City, Taguig, PH, Philippines
- Anson, Jose Maria L., SLMC, Saint Luke's Medical Center - Global City, Taguig, PH, Philippines
Group or Team Name
- Center for Renal Diseases.
Introduction
HIV patients face renal risks from viral effects, ART toxicity, and drug use. Amphetamines can cause AKI via rhabdomyolysis or AIN, but their link to immune complex GN is unclear. We present a rare biopsy-proven case of both GN and AIN in an HIV-positive patient post-amphetamine use.
Case Description
A 34-year-old Filipino male with HIV (CD4 283; viral load 60), on lamivudine/tenofovir/dolutegravir, presented with AKI after recent amphetamine use, with severe low back pain, tea-colored urine, and oliguria. Labs showed creatinine 6.4 mg/dL, eGFR 11 mL/min, proteinuria, and hematuria. Ultrasound showed increased renal echogenicity without obstruction. Biopsy revealed immune complex-mediated glomerulonephritis (IgG, IgM, C3, C1q) and acute interstitial nephritis. EM showed podocyte foot process effacement without dense deposits. This case illustrates multifactorial AKI in HIV and the value of early biopsy.
Discussion
This case illustrates a complex, multifactorial renal insult in an HIV-positive patient. While amphetamines are associated with AIN, the concurrent immune complex GN raises the possibility of drug-induced immune activation in the setting of HIV-mediated immune dysregulation. The absence of classical lupus-like features and lack of significant electron-dense deposits argue against HIVAN or lupus nephritis.
18 glomeruli (2 sclerosed), IgG/IgM/fibrinogen (trace), IgA/C1q (1-2+), C3 (2-3+), vascular (2+).
EM showed diffuse podocyte foot process effacement, with no definite electron-dense deposits or tubuloreticular inclusions