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

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

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Journal
Journal of the American Society of Nephrology
Published
2025-10-01
DOI
https://doi.org/10.1681/asn.2025ye2j19aj
Primary Topic
Kidney Stones and Urolithiasis Treatments
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article
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article

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

Yaman Mazen Almerstani, Reem Daloul, Kalathil K. Sureshkumar, Khaled Nashar et al.
Journal of the American Society of Nephrology
Kidney Stones and Urolithiasis Treatments
article

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

Yaman Mazen Almerstani, Reem Daloul, Kalathil K. Sureshkumar, Khaled Nashar, Ahmed Barazi, Manuel A. Valle Moradel
article en

Abstract

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

Journal of the American Society of NephrologyVol. 36(10S)
Allegheny Health Network (US)
Openalex Percentile: Top 52%
Kidney Stones and Urolithiasis Treatments
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