Abstract: SA-PO0768
When the Great Mimicker Meets the Great Hepatic Villain: Non-Lupus Full-House Nephropathy in the Setting of Chronic Hepatitis C and Treated Latent Syphilis
Session Information
- Glomerular Diseases: Lupus Nephritis, Monoclonal Gammopathy-Related Disease, and Transplantation
October 24, 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
- Iftikhar, Muhammad Ali, Edward Hines Junior Veterans Affairs Hospital, Hines, Illinois, United States
- Joseph, Thomas, Edward Hines Junior Veterans Affairs Hospital, Hines, Illinois, United States
- Wadhwa, Anuradha, Edward Hines Junior Veterans Affairs Hospital, Hines, Illinois, United States
Introduction
Full-house nephropathy (FHN) — glomerular co-deposition of IgG, IgA, IgM, C3, and C1q — is classically considered pathognomonic of lupus nephritis. Non-lupus FHN (NLFHN) is rare; published series cite HIV and Bartonella as predominant infectious etiologies, with HCV notably absent. Syphilis is increasingly recognized as producing full-house immunofluorescence, often misattributed to lupus. We report NLFHN with concurrent active HCV and treated latent syphilis as competing etiologic contributors.
Case Description
A 72-year-old African American male with chronic HCV, treated latent syphilis (penicillin completed 2025, likely serofast), and hypertension presented with rapidly progressive CKD: creatinine 1.4 mg/dL (eGFR 54) in 10/2024, rising to 5.87 (eGFR 10) by 12/2025 and 10 mg/dL (eGFR 5) by 03/2026. Biopsy (11/2025) showed immune complex GN with mesangial proliferation, segmental endocapillary hypercellularity, and hypertensive arterionephrosclerosis. Immunofluorescence: IgG 1–2+, IgA 1–2+, IgM 1–2+, C1q 2+, kappa 2+, lambda 2+, C3 trace. Serology: ANA 1:180, anti-dsDNA positive, C3 30.6 (low), C4 normal, RPR 1:8, cryoglobulins negative, anti-PLA2R negative. No SLE criteria met. HCV treatment with glecaprevir/pibrentasvir is ongoing.
Discussion
HCV drives non-cryoglobulinemic immune complex GN via mesangial IC deposition, absent from NLFHN literature. Concurrently, whether persistent low-titer RPR in treated serofast patients reflects residual treponemal antigenemia sufficient to perpetuate IC deposition remains biologically unresolved — this case raises that question in the context of NLFHN. Positive anti-dsDNA and low C3 without SLE criteria likely reflect infection-driven polyclonal immune activation seen in both HCV and treponemal disease; normal C4 argues against classical complement activation of lupus. To our knowledge, this combination is unreported.
This case illustrates that FHN is not exclusive to lupus. HCV and treated latent syphilis may simultaneously drive NLFHN via immune complex deposition. Whether serofast-state treponemal immune activity contributes to renal IC deposition is an unresolved question. Positive anti-dsDNA likely reflects infection-driven immune activation rather than SLE. Renal biopsy is essential in HCV-infected patients with progressive CKD to guide diagnosis and avoid empiric immunosuppression.