Abstract: FR-PO0688
Seroconversion in Membranous Nephropathy: From Seronegative to Seropositive Disease
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
- Preuss, Kiersten M., University of Nebraska Medical Center College of Medicine, Omaha, Nebraska, United States
- Trappett, Kevin Paul, University of Nebraska Medical Center, Omaha, Nebraska, United States
- Talmon, Geoffrey, University of Nebraska Medical Center, Omaha, Nebraska, United States
- Foster, Kirk W., University of Nebraska Medical Center, Omaha, Nebraska, United States
- Benes, Brian Joseph, University of Nebraska Medical Center, Omaha, Nebraska, United States
Introduction
Membranous nephropathy (MN) is increasingly classified by target antigens, with anti-phospholipase A2 receptor (PLA2R) antibodies being the most common. In transplant recipients, the PLA2R status is vital for risk stratification. However, the negative predictive value of the serology is approximately 50% and according to KDIGO 2021 guidelines, antibodies may reappear post-transplant. We present a renal transplant recipient who developed PLA2R negative MN with delayed PLA2R seroconversion occurring eight years after first MN diagnosis, leading to reclassification of his MN.
Case Description
A 66-year-old man with end-stage kidney disease of unknown etiology and first allograft failure due to chronic rejection, received a second kidney transplantation nine years after his first. After five years of stable allograft function and a self-reduction of immunosuppression, he developed nephrotic-range proteinuria (UPCR>10 g/g). Renal allograft biopsy showed early MN with negative PLA2R staining and mild acute cellular rejection. While peritubular C4d staining was negative, glomerular C4d was positive in the MN lesions. After two doses of rituximab, his UPCR improved and he was then lost to follow-up.
Eight years later, the patient presented with acute allograft dysfunction and nephrotic-range proteinuria (UPCR >12 g/g). He reported self-discontinuing his immunosuppression due to side effect intolerance. Repeat biopsy confirmed MN but serologic evaluation now demonstrated newly positive anti-PLA2R antibodies. He was re-initiated on mycophenolate mofetil and rituximab prior to relocating and lost to follow-up.
Discussion
This case highlights the limitations of single time-point serologic assessment in MN and suggests that seroconversion may reflect several mechanisms, including evolving immune mechanisms or alloimmune triggers in the transplant setting. Inadequate immunosuppression is a proposed trigger for MN. Alternatively, the circulating PLA2R levels could be below the detection threshold of the assay, consistent with the early-stage MN lesions found histologically and suggesting low-level disease activity. Our experience highlights the role of longitudinal monitoring of PLA2R antibodies, even in cases with an initial negative result, for accurate classification and management of renal allograft recipients.