Abstract: SA-PO1194
Recurrent Oxalate Nephropathy and Early Kidney Allograft Failure
Session Information
- Transplantation: Clinical - Complications, Pediatrics, and Multi-Organ Considerations
October 24, 2026 | Location: Exhibit Hall A, Convention Center
Abstract Time: 10:00 AM - 12:00 PM
Category: Transplantation
- 2002 Transplantation: Clinical
Authors
- Gutierrez, Omar, The Ohio State University, Columbus, Ohio, United States
- Moustafa, Amr, The Ohio State University, Columbus, Ohio, United States
- Satoskar, Anjali A., The Ohio State University, Columbus, Ohio, United States
- Singh, Priyamvada, The Ohio State University, Columbus, Ohio, United States
- Cholin, Liza, The Ohio State University, Columbus, Ohio, United States
Introduction
Oxalate nephropathy after kidney transplantation is a rare but important cause of allograft dysfunction, particularly in patients with enteric hyperoxaluria. We report a case of oxalate nephropathy recurrence post-transplant that was resistant to medical therapy and led to early allograft loss.
Case Description
A 73-year-old female with end-stage kidney disease (ESKD) secondary to calcium oxalate crystal deposition, in the setting of Crohn's disease requiring partial colectomy, underwent a deceased donor kidney transplant with a kidney donor profile index (KDPI) of 92%. Her post-operative course was complicated by DGF requiring dialysis. Serum oxalate levels rose post-operatively from 17.5 μmol/L on day 2 to 47.8 μmol/L on day 11. An allograft biopsy on day 15 showed severe acute tubular necrosis (ATN) and numerous (3+) intratubular calcium oxalate crystals without evidence of rejection. Her subsequent course included severe diarrhea (up to 22 bowel movements/day); a colonoscopy ruled out a Crohn's flare, thus pointing towards mycophenolate toxicity. Her diarrhea resulted in oxalate hyperabsorption and highly variable, supra-therapeutic tacrolimus levels. Despite mycophenolate avoidance and aggressive medical management of the hyperoxaluria, the patient developed rapid allograft fibrosis (45% by month 4) and graft loss.
Discussion
This case illustrates the risk of recurrent oxalate nephropathy in recipients with enteric hyperoxaluria. It demonstrates a notable challenge in post-transplant management: standard immunosuppression (mycophenolate) caused gastrointestinal toxicity, which exacerbated the underlying hyperoxaluria and destabilized calcineurin inhibitor pharmacokinetics, contributing to crystal deposition and graft scarring.
Teaching points:
1. Recurrent oxalate nephropathy can occur early after transplant in patients with enteric hyperoxaluria, especially when diarrhea increases oxalate absorption.
2. GI toxicity from mycophenolate can worsen hyperoxaluria and destabilize tacrolimus levels, accelerating allograft injury.