Abstract: TH-PO0914
Pauci-Immune Glomerulonephritis: An Uncommon Cause of Early Post-Transplant Kidney Allograft Dysfunction
Session Information
- Transplantation: Clinical - Glomerular Diseases, Infections, and Rejection
November 06, 2025 | Location: Exhibit Hall, Convention Center
Abstract Time: 10:00 AM - 12:00 PM
Category: Transplantation
- 2102 Transplantation: Clinical
Authors
- Younis, Sherif Elbaz, HCA Healthcare Graduate Medical Education, Kingwood, Texas, United States
- Castaneda, Andy Bryan, University of Houston Tilman J Fertitta Family College of Medicine, Houston, Texas, United States
- Valdes, Jose Luis, DHR Health Transplant Institute, McAllen, Texas, United States
- Allam, Sridhar Reddy, DHR Health Transplant Institute, McAllen, Texas, United States
Introduction
Antineutrophil cytoplasmic antibody (ANCA) associated vasculitis (AAV) has low rates of recurrence post kidney transplant due to potent antirejection regimens. Early recurrence is rare. Here in, we present a case of early post transplant recurrent AAV
Case Description
A 70-year-old woman with a history of end-stage kidney disease reportedly secondary to post-streptococcal glomerulonephritis (GN) and hypertension who had been dialysis dependent for about 3 years presented for a kidney transplant. Her history of post-streptococcal GN was unclear with lack of records and required treatment with steroids and plasma exchange over 20 years ago. She received a kidney from a 48 year deceased donor who had hypertension and died of stroke. She was given thymoglobulin induction followed by a triple immunosuppressive regimen of tacrolimus, mycophenolate and prednisone. She had immediate allograft function with nadir serum creatinine of 1.9 mg/dL by post operative day 10. However, serum creatinine increased to 2.7 mg/dL with persistent microscopic hematuria and a random urine albumin to creatinine ratio of 2.1 by post operative day 20. Allograft biopsy revealed pauci-immune crescentic GN (PIGN), characterized by extensive necrosis or crescent formation in 12 out of 13 glomeruli. Serologies revealed positive ANCA screen with p-ANCA titer of 1:320. She received treatment with intravenous pulse steroids and rituximab with stabilization of kidney function and proteinuria.
Discussion
Cases of rapidly progressing post-transplant PIGN have been reported before, with the mean time to biopsy diagnosis typically ranging from months to years post-transplant. Our patient developed PIGN within one month after transplant, emphasizing that PIGN can manifest any time during the post-transplant period. This underscores the necessity for clinicians to identify etiology of native kidney disease prior to transplant and maintain a broad differential including PIGN, especially in those transplant recipients with no clearly documented etiology of native kidney disease presenting with early allograft dysfunction and/or worsening proteinuria, to ensure timely diagnosis and management.