Abstract: FR-PO0743
Allograft Recurrence of COVID-19-Associated Seronegative Membranous Nephropathy: Codominant IgA/IgG Deposits and Lectin Complement Pathway Activation
Session Information
- Glomerular Diseases: ANCA Vasculitis, Anti-GBM Disease, and Crescentic GN
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
- Younis, Nour Khaled, The University of Texas Southwestern Medical Center, Dallas, Texas, United States
- Saxena, Ramesh, The University of Texas Southwestern Medical Center, Dallas, Texas, United States
Introduction
COVID-19 infection has been temporally associated with the development of de novo membranous nephropathy (MN), with onset typically occurring within weeks to months of infection. The pathogenesis of COVID-19-triggered MN, particularly de novo seronegative MN, and its behavior following renal transplantation remain poorly understood. We report an unusual case of treatment-resistant MN recurring in a renal allograft following COVID-19-associated disease.
Case Description
A 56-year-old male with coronary artery disease, hypertension, and hyperlipidemia, developed nephrotic-range proteinuria (UPCR 10.4 g/g), creatinine 2.89 mg/dL (eGFR 25), and no hematuria approximately 3–4 months after COVID-19 infection. Serum PLA2R antibodies were negative. Native kidney biopsy showed MN with weakly positive tissue PLA2R, mild IFTA (5%), and IF demonstrating co-dominant IgA/IgG, C3, and C1q — consistent with classical complement pathway activation. Despite receiving rituximab and tacrolimus, he had persistent proteinuria and progressive renal decline.
Patient underwent living donor kidney transplantation with thymoglobulin induction and standard maintenance (tacrolimus, MMF, prednisone). MN recurred in the allograft within 4 months. Allograft biopsy again demonstrated co-dominant IgA/IgG deposits; however, C3 and C4d were present without C1q, indicating a shift to lectin rather than classical complement pathway activation. Disease remains resistant to treatment.
Discussion
This case highlights the diagnostic complexity of seronegative MN with atypical IF patterns in the context of COVID-19. While MN superimposed on IgA nephropathy is possible, recurrence of the identical co-dominant IgA/IgG pattern in the allograft strongly supports a persistent systemic autoimmune process triggered by COVID-19-induced immune dysregulation. The shift from classical (C1q+) to lectin pathway (C4d+, C1q−) complement activation in the allograft may reflect altered post-transplant immune dynamics; this complement shift may explain rituximab resistance, as lectin pathway activation is independent of B-cell-mediated immunity. This case suggests that COVID-19-associated MN may represent a distinct pathological entity that does not conform to the usual paradigm of primary MN, pointing toward complement-targeted therapy as a rational next step in refractory disease.