Abstract: TH-PO0919
Is Peritoneal Dialysis a Barrier to Kidney Transplant in Roux-en-Y Gastric Bypass-Associated Hyperoxalemia?
Session Information
- Home Dialysis: Utilization Patterns, Complications, and Quality-of-Life Outcomes
October 22, 2026 | Location: Exhibit Hall A, Convention Center
Abstract Time: 10:00 AM - 12:00 PM
Category: Dialysis
- 802 Dialysis: Home Dialysis and Peritoneal Dialysis
Authors
- Bhatti, Muhammad Muaz, Mayo Clinic in Florida, Jacksonville, Florida, United States
- Mao, Michael A., Mayo Clinic in Florida, Jacksonville, Florida, United States
- Batish, Ishaan, Mayo Clinic in Florida, Jacksonville, Florida, United States
- Bobart, Shane A., Mayo Clinic in Florida, Jacksonville, Florida, United States
- Aslam, Nabeel, Mayo Clinic in Florida, Jacksonville, Florida, United States
Introduction
Enteric hyperoxaluria after Roux-en-Y gastric bypass (RYGB) can cause nephrolithiasis and oxalate nephropathy, leading to end stage kidney disease (ESKD). Many transplant programs do not accept ESKD patients with RYGB for kidney transplantation if the plasma oxalate level is >30umol/L due to concern for oxalate deposition with resultant allograft failure. We present two cases of ESKD on peritoneal dialysis (PD), with RYGB associated hyperoxalemia, who were denied kidney transplant due to persistent oxalate >30umol/L while on PD requiring switching to intensive hemodialysis (HD).
Case Description
Patient 1: A 62-year-old female with morbid obesity s/p RYGB presented with AKI (Creatinine 10.2 mg/dL from a baseline of 0.8 mg/dL). Kidney biopsy showed features consistent with oxalate nephropathy, and the patient chose PD for renal replacement therapy. Despite low-oxalate diet, use of oxalate binding agents including calcium and cholestyramine, and intensification of PD regimen over 24 months, the plasma oxalate remained elevated up to 51.7 μmol/L. She was denied activation on transplant list due to hyperoxalemia. She was switched to home HD 4 times/week and oxalate improved to 23.7 μmol/L after 12 months of intensive HD.
Patient 2: A 44-year-old female with diabetes, hypertension, obesity s/p RYGB, and ESKD due to DM/HTN chose PD for renal replacement therapy. She remained inactive on kidney transplant list due to high oxalate levels up to 54.5 μmol/L despite low oxalate diet, calcium carbonate with meals, and intensification of PD regimen. She transitioned to in-center HD after 18 months on PD to improve oxalate clearance. Oxalate improved to 13.6 μmol/L after 9 months of intensive HD after which she successfully received a kidney transplant.
Discussion
These cases suggest that PD may provide insufficient oxalate clearance in selected transplant candidates with RYGB-associated hyperoxalemia. Persistent systemic oxalate burden can delay kidney transplant due to concern for post-transplant oxalate nephropathy. Conversion to intensive HD was associated with meaningful oxalate reduction in both patients and successful transplantation in one. These cases highlight that PD may not be the preferred dialysis modality for ESKD patients with RYGB associated hyperoxalemia. Persistent hyperoxalemia on PD should prompt early reassessment of dialysis modality with consideration of intensive HD.