Abstract: FR-PO0784
Recurrent FSGS Due to Anti-Nephrin Antibodies After Kidney Transplantation: A Case Report
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
- Ghimire, Sandip, Geisinger Medical Center, Danville, Pennsylvania, United States
- Sanghi, Pooja, Geisinger Medical Center, Danville, Pennsylvania, United States
Introduction
Recurrent FSGS occurs in approximately 50% of transplant recipients whose native disease was not FSGS. Anti-nephrin antibodies play pathogenic role in this immune-mediated podocytopathy. We report recurrent anti-nephrin–associated FSGS post-kidney transplantation, treated with plasmapheresis, rituximab, and daratumumab.
Case Description
A 55-year-old male received DCD kidney transplant (July 2025) for biopsy-proven hypertensive nephrosclerosis with pre-transplant proteinuria of 3g. He received standard ATG induction and CNI-based IS. One-month post-transplant, proteinuria rose to 6 g, rapidly escalating to 19 g. Allograft biopsy showed FSGS with collapsing features and borderline acute TCMR. Initial treatment with PLEX, prednisone, and rituximab reduced proteinuria to 4.5g, but it rebounded to 10g after 19 PLEX sessions. Given refractory disease, pre-transplant serum was sent to a major outside research center, which tested positive for anti-nephrin antibodies. Daratumumab was initiated as rescue therapy; after 2 doses 8 weeks apart, proteinuria decreased to 2.75 g — first subnephrotic level since diagnosis. CNI was stopped due to intolerance, and was transitioned to monthly belatacept, MMF, and low-dose prednisone. On last follow-up, proteinuria rose to 6.2 g; weekly PLEX continues with 2 additional daratumumab doses planned. Allograft function remains stable (cr 1.1, eGFR 78).
Discussion
Anti-nephrin Ab can drive recurrent FSGS post-transplant even without prior glomerular disease. CD38+ plasma cells producing these Ab can be targeted with daratumumab, providing complete B-cell lineage depletion. PLEX, steroids, and rituximab alone were insufficient; adding daratumumab achieved meaningful proteinuria reduction. Variability in dosing regimens and limited Ab testing availability remain challenges. Anti-nephrin Ab testing should be considered in post-transplant proteinuria regardless of original disease. Anti-CD38 therapy may be considered in refractory cases after expert consultation.
Trend of Urine ACR After Kidney Tx