Abstract: FR-PO0693
When Autoantibodies Mislead: Biopsy-Proven Collapsing HIV-Associated Nephropathy Mimicking Autoimmune Glomerulonephritis
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
- Ravulapalli, Madhavi, Centinela Hospital Medical Center, Inglewood, California, United States
- Tavaratsyan, Ani, Centinela Hospital Medical Center, Inglewood, California, United States
- Arain, Fatima H., Centinela Hospital Medical Center, Inglewood, California, United States
- Dantuluri, Sahitya, Centinela Hospital Medical Center, Inglewood, California, United States
- Pak, Firooz, Centinela Hospital Medical Center, Inglewood, California, United States
Introduction
Advanced HIV infection causes immune dysregulation with broad autoantibody production that may mimic systemic autoimmune disease. Distinguishing true autoimmune glomerulonephritis from HIV-associated nephropathy (HIVAN) is critical, as management differs substantially.
Case Description
A 36-year-old woman with hidradenitis suppurativa and prior deep vein thrombosis presented with abdominal pain, diarrhea, and oliguria. Laboratory evaluation revealed severe acute kidney injury (creatinine 7.0 mg/dL from baseline 0.8 mg/dL), hemoglobin 4.6 g/dL, thrombocytopenia, metabolic acidosis, nephrotic-range proteinuria, and active urine sediment. Imaging demonstrated diffuse lymphadenopathy and a small pericardial effusion.
Serologic testing showed broad autoantibody positivity, including ANA, anti-histone, anti-RNP, low-titer c-ANCA, and triple-positive antiphospholipid antibodies (anticardiolipin IgG/IgM, lupus anticoagulant, positive dilute Russell viper venom time). Complement levels (C3 and C4) were normal. Given concern for autoimmune rapidly progressive glomerulonephritis, high-dose corticosteroids were initiated.
Further evaluation revealed advanced HIV infection with CD4 count 34 cells/µL, and antiretroviral therapy was started. Kidney biopsy demonstrated collapsing focal segmental glomerulosclerosis with severe acute tubular necrosis and extensive interstitial fibrosis, without immune complex deposition, necrotizing lesions, crescents, or thrombotic microangiopathy. Immunosuppression was discontinued, and the diagnosis was revised to HIV-associated nephropathy with serologic epiphenomena. Renal recovery did not occur, and the patient required maintenance hemodialysis.
Discussion
This case illustrates how advanced HIV can generate extensive autoantibody positivity—including ANA, ANCA, and triple-positive antiphospholipid antibodies—mimicking lupus nephritis, ANCA-associated vasculitis, and antiphospholipid syndrome nephropathy. Normal complement levels and absence of immune complex or necrotizing pathology on biopsy were decisive. Early HIV testing and kidney biopsy are essential before committing to immunosuppression in patients with rapidly progressive kidney injury and extensive serologic activation.