Abstract: SA-PO0993
When IgA Strikes Twice: The Battle Beyond Transplant
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
- Khan, Salwa, West Virginia University, Morgantown, West Virginia, United States
- Danforth, Jessie, West Virginia University, Morgantown, West Virginia, United States
- Mareedu, Neeharik, UPMC, Pittsburgh, Pennsylvania, United States
- Agarwal, Krishna A., West Virginia University, Morgantown, West Virginia, United States
Introduction
IgA nephropathy (IgAN) is a leading cause of end-stage kidney disease (ESKD) and can recur in kidney allografts, potentially affecting graft survival. Currently, there is no standardized treatment for post-transplant recurrence of IgAN, and management remains challenging. Clinical trials for newer therapies have excluded kidney transplant recipients.
Case Description
A 40-year-old female with ESKD secondary to biopsy-confirmed IgAN underwent a deceased-donor kidney transplant. 11-months post-transplant, she developed asymptomatic hematuria, worsening proteinuria (1.9 g/g from 0.5-0.7g/g), and an increase in serum creatinine to 2.0 mg/dL (from 1.1-1.4mg/dL). Allograft biopsy demonstrated mesangial IgA deposition consistent with recurrent IgAN (M1E0S1T0C0).
Initial management included losartan 100 mg daily, which led to a modest improvement in proteinuria (1.2 g/g) and creatinine (1.7 mg/dL). She was also on semaglutide 2 mg/wk for diabetes mellitus.
Despite supportive therapy, proteinuria worsened to 3.5-4g/g over the following year. Targeted-release budesonide (TRF-budesonide; Tarpeyo) was initiated at 16mg/d in addition to standard triple immunosuppression and resulted in a significant reduction in proteinuria (0.9g/g), resolution of hematuria, and stabilization of allograft function over 4 months (Figure). Dose was then reduced to 8mg/d for worsened hypertension. No infectious adverse events were noted.
Discussion
Up to 50% of kidney transplant recipients (KTR) will have recurrence of IgAN post-transplantation and 20-40% will progress to ESKD. Landmark trials for newer IgAN therapies have excluded KTRs. This case highlights the potential role of TRF-budesonide in the management of recurrent IgAN post-transplant. Its targeted mechanism at the gut mucosal immunity provides the necessary immunosuppressive effect while avoiding additional systemic immunosuppression in this high-risk population. We encourage clinical trials to establish long-term efficacy and safety in the transplant population.