Abstract: SA-PO1032
Recurrent Anti-Phospholipase A2 Receptor-Associated Membranous Nephropathy Post-Kidney Transplantation After Complete Remission
Session Information
- Transplantation: Clinical - Case Reports
November 08, 2025 | Location: Exhibit Hall, Convention Center
Abstract Time: 10:00 AM - 12:00 PM
Category: Transplantation
- 2102 Transplantation: Clinical
Authors
- Michael, Sean, University of Florida, Gainesville, Florida, United States
- Belal, Amer Ashaab, University of Florida, Gainesville, Florida, United States
- Clapp, William L., University of Florida, Gainesville, Florida, United States
- Santos, Alfonso, University of Florida, Gainesville, Florida, United States
- Leghrouz, Muhannad, University of Florida, Gainesville, Florida, United States
Introduction
Anti-phospholipase A2 receptor antibodies (anti-PLA2R) are detected in 70-80% of patients with primary membranous nephropathy (pMN). The presence of pretransplant anti-PLA2R increases the risk of recurrent anti-PLA2R MN post KT but might be not associated with disease activity post KT.
Case Description
A 51-year-old male with kidney failure due to anti-PLA2R MN who received a cadaveric KT presents with worsening proteinuria. Serum anti-PLA2R titer (IFA) was 1:2560 at listing 6 months prior to KT. Induction was with Alemtuzumab and maintenance with Tacrolimus (TAC), Mycophenolate (MMF), and Prednisone. His post KT course was complicated by DGF, followed by hypogammaglobinemia and disseminated Nocardia 2 months post KT treated with long-term antibiotics, reduction in TAC, and withdrawal of MMF. 6 weeks post KT he started to have worsening proteinuria. Donor-derived cell-free DNA was 0.43% with absent donor-specific antibodies. Given anti-PLA2R titer 1:80, recurrent MN was presumed. Due to active disseminated Nocardia precluding therapy, KT biopsy was deferred. He was conservatively managed with Losartan. By 12 months post KT patient had complete (clinical and serological) remission with serum creatinine (SCr) 1.7-1.9 mg/dl (baseline), urine PCR down to 70 mg/g, and undetected anti-PLA2R. Patient started again to have worsening albuminuria and proteinuria 3760 mg/g and 4290 mg/g, respectively with SCr up to 2.2 mg/dl at 16 months post KT. Anti-PLA2R remained undetected. KT biopsy yielded findings consistent with PLA2R-positive MN (Figure 1). The patient received Rituximab with improved SCr and proteinuria.
Discussion
This case of anti-PLA2R MN recurring after complete remission post KT is illustrative of evaluating proteinuria and kidney function with KT biopsy to monitor disease activity rather than solely relying upon anti-PLA2R titer. Literature supports the correlation of anti-PLA2R levels with disease activity and remission before KT and with recurrence post KT. However, data on anti-PLA2R to monitor disease activity in recurrent anti-PLA2R MN post KT is limited.