Abstract: FR-PO0697
When Phospholipase A2 Receptor Meets Hepatitis B: Navigating Primary vs. Secondary Membranous Nephropathy
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
- Khan, Noorelle, MedStar Health-Georgetown/Washington Hospital Center Residency Program in Internal Medicine, Washington, District of Columbia, United States
- Thach, Lonnie, MedStar Washington Hospital Center, Washington, District of Columbia, United States
- Nasr, Samih H., Mayo Clinic Minnesota, Rochester, Minnesota, United States
Introduction
Membranous nephropathy (MN) is a common cause of nephrotic syndrome in adults. Most cases are primary and associated with antibodies against phospholipase A2 receptor (PLA2R). Hepatitis B virus (HBV) is a recognized secondary cause of MN; however, PLA2R positivity has also been reported in HBV-associated MN, creating diagnostic and therapeutic uncertainty.
Case Description
A male in his 60s with biopsy-proven PLA2R-positive MN, CKD stage IIIb, hypertension, diabetes mellitus, and heart failure with preserved ejection fraction presented with progressive anasarca and 20 pound weight gain over three months. Laboratory evaluation showed nephrotic-range proteinuria (13 g/g), hypoalbuminemia (2.6 g/dL), and stable chronic kidney dysfunction. Rituximab was planned for high-risk MN; however, pre-treatment screening revealed active HBV infection with positive HBsAg, HBeAg and HBV DNA >20,000 IU/mL.
Due to concern for HBV-associated MN and risk of viral reactivation with immunosuppression, tenofovir was initiated. Despite reduction of HBV viral load to <50 IU/mL, proteinuria and edema persisted. The patient was transitioned to entecavir for viral suppression and subsequently cleared for immunosuppression. Tacrolimus was initiated for interim control of severe nephrotic syndrome, followed by rituximab with Pneumocystis jirovecii prophylaxis. The patient subsequently demonstrated improvement in edema while maintaining viral suppression.
Discussion
PLA2R antibodies while specific for primary MN have also been described in HBV-associated MN. HBV-MN often improves with antiviral therapy alone, whereas primary MN typically requires immunosuppression. In this case, persistent nephrotic syndrome despite viral suppression suggested that PLA2R-mediated primary MN was the predominant driver of disease. This case highlights the importance of individualized management and careful sequencing of antiviral and immunosuppressive therapy to reduce HBV reactivation risk while treating progressive nephrotic syndrome.
Figure 1: Renal biopsy with immunofluorescense showing PLA2R positivity