Kidney Week

Abstract: SA-PO0978

Acute Oxalate Nephropathy: An Unusual Cause of Early Post-Transplant Kidney Allograft Dysfunction and Favorable Outcome with Prompt Intervention

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

• Almerstani, Yaman Mazen, Allegheny Health Network, Pittsburgh, Pennsylvania, United States

Yaman Mazen Almerstani, MD

• Valle Moradel, Manuel A., Allegheny Health Network, Pittsburgh, Pennsylvania, United States

Manuel A. Valle Moradel, MD

• Barazi, Ahmed, Allegheny Health Network, Pittsburgh, Pennsylvania, United States

Ahmed Barazi, MD

• Nashar, Khaled, Allegheny Health Network, Pittsburgh, Pennsylvania, United States

Khaled Nashar, MD, FASN

• Daloul, Reem, Allegheny Health Network, Pittsburgh, Pennsylvania, United States

Reem Daloul, MD

• Sureshkumar, Kalathil K., Allegheny Health Network, Pittsburgh, Pennsylvania, United States

Kalathil K. Sureshkumar, MD, FASN

Introduction

Kidney allograft dysfunction in the early post-transplant period results from multitude of causes. We present a patient who developed early post-transplant acute oxalate nephropathy with favorable response to prompt medical therapy.

Case Description

A 59-year-old male (EBV and CMV IgG +ve) with hypertension, Roux en Y gastric bypass (RYGB) 6 years earlier and orthotopic liver transplantation one year earlier complicated by dialysis dependence underwent deceased donor kidney transplantation from a 34-year-old brain dead donor (EBV IgG +ve and CMV IgG -ve) by using basiliximab and methyl prednisolone induction followed by tacrolimus/mycophenolic acid maintenance and standard infection prophylaxis. There was prompt allograft function with a nadir serum creatinine of 0.81 mg/dL 2 weeks later but started increasing at 6-week point from transplant and peaked at 2.22 mg/dL. Allograft ultrasound with Doppler was unremarkable and biopsy showed acute oxalate nephropathy (figure). Serum oxalate level was sent, and patient underwent 3 days of dialysis to lower oxalate level. He was instructed to follow a low-oxalate diet, adequate hydration and was prescribed calcium carbonate as gut oxalate binder. Initial serum oxalate level was 14 mcmol/L (1.3-3.1) but decreased to 2.7 mcmol/L two weeks later and undetectable in subsequent weeks. Serum creatinine started to improve with a value of 1.27 mg/dL at last follow up 3 months later.

Discussion

RYGB can result in enteric hyperoxaluria, low urinary calcium and citrate and possibly low urine volume from gut losses, factors predisposing to oxalate nephropathy and kidney stones. A high index of suspension, early diagnosis and prompt intervention can prevent irreversible allograft injury. Surgical reversal of RYGB may be required in some patients. In high-risk patients, pre transplant dialysis and post-transplant monitoring of serum oxalate levels with medical therapy could reduce risk for allograft oxalate nephropathy.

1a. Calcium oxalate crystals in tubules, b. Polarized crystal. c.Sunburst architecture of crystal and surrounding giant cell reaction

Digital Object Identifier (DOI)

• doi: 10.1681/ASN.2025ye2j19aj