Abstract: FR-PO0943
HIV Mimicking Lupus Nephritis: A Diagnostic Challenge
Session Information
- Glomerular Case Reports: Lupus, FSGS, Complement, and More
November 07, 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
- Hti Lar Seng, Nang San, Beth Israel Deaconess Medical Center, Boston, Massachusetts, United States
- Stowe, Ifeoluwa Toyin, Beth Israel Deaconess Medical Center, Boston, Massachusetts, United States
- Kavcar, Akil Serdar, Beth Israel Deaconess Medical Center, Boston, Massachusetts, United States
- Hirpara, Samir, Beth Israel Deaconess Medical Center, Boston, Massachusetts, United States
- Rennke, Helmut G., Brigham and Women's Hospital, Boston, Massachusetts, United States
- William, Jeffrey H., Beth Israel Deaconess Medical Center, Boston, Massachusetts, United States
Introduction
While HIV-associated nephropathy (HIVAN), often characterized by collapsing focal segmental glomerulosclerosis, is the most common HIV-related glomerular disease, HIV can also present with immune complex glomerulonephritis (GN) that mimics lupus nephritis both histologically and serologically. This can result in misdiagnosis and inappropriate immunosuppression.
Case Description
A 31-year-old male with no significant medical history presented with three weeks of gross hematuria, right flank pain, and bilateral lower extremity edema. He had recently started creatine supplements but denied rash or arthralgia. Blood pressure was 148/91 mmHg, and other vitals were normal. Physical exam revealed only pedal edema. Labs showed serum creatinine 1.9 mg/dL, urinalysis with 26 WBCs, 182 RBCs, and protein-creatinine ratio of 1.9 g/g. Urine sediment had acanthocytes and mostly isomorphic red blood cells. Serologic workup revealed ANA 1:160, dsDNA >300 IU/mL, low C3 (75 mg/dL), normal C4 (20 mg/dL), and negative ANCA, anti-GBM, anti-Smith, RNP, SSA/SSB. ESR and CRP were normal.
Renal biopsy showed diffuse proliferative GN with full-house immune complex deposition, consistent with class IV lupus nephritis, along with moderate acute interstitial nephritis. The patient was treated with pulse methylprednisolone and mycophenolate mofetil. Despite therapy, kidney function declined, and he required hemodialysis by day 10 of hospitalization. Subsequent HIV testing returned positive with viral load 3.1 log copies/mL and CD4 count 297 cells/μL. In the absence of clinical features of systemic lupus erythematosus (SLE), the diagnosis was revised to HIV-associated immune complex GN with lupus-like features. Immunosuppression was discontinued, antiretroviral therapy (Biktarvy) was initiated, and prednisone was tapered. However, renal recovery did not occur, and the patient is undergoing transplant evaluation.
Discussion
This case underscores the ability of HIV to mimic lupus nephritis and the importance of including HIV in the differential diagnosis of immune complex GN. Early HIV testing is crucial to avoid misdiagnosis and unnecessary immunosuppression, which can be harmful in immunocompromised patients. Management of HIV-related GN should prioritize antiretroviral therapy over immunosuppressive regimens.