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Updated: Jun 28, 2026

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Published on: April 28, 2013
Acute oxalate nephropathy causing late renal transplant dysfunction due to enteric hyperoxaluria
A C Rankin1, S B Walsh, S A Summers
1Renal Department, King's College London School of Medicine, London, UK. rankinalex@yahoo.com
Enteric hyperoxaluria from pancreatic insufficiency caused late kidney transplant dysfunction. Prompt treatment with enzyme supplements, dialysis, and diet improved graft function, highlighting the need to consider malabsorption in transplant patients with diarrhea and declining kidney function.
Area of Science:
- Nephrology
- Gastroenterology
- Transplantation
Background:
- Calcium oxalate (CaOx) deposition is a significant cause of kidney allograft injury.
- Enteric hyperoxaluria, often linked to malabsorption, can lead to CaOx nephropathy.
- Pancreatic insufficiency can result in fat malabsorption and subsequent enteric hyperoxaluria.
Observation:
- A kidney transplant recipient presented with late graft dysfunction and diarrhea.
- The patient had a history of noncompliance with pancreatic enzyme replacement therapy.
- This led to a diagnosis of enteric hyperoxaluria secondary to pancreatic insufficiency.
Findings:
- Acute oxalate nephropathy was diagnosed in the renal allograft.
- Treatment involved hemodialysis, a low-fat, low-oxalate diet, and pancreatic enzyme supplementation.
- The patient's graft function recovered following the intervention.
Implications:
- Fat malabsorption leading to enteric hyperoxaluria should be considered in renal transplant recipients with diarrhea and graft dysfunction.
- Ensuring compliance with pancreatic enzyme replacement therapy is crucial for patients with pancreatic insufficiency.
- Early recognition and management of enteric hyperoxaluria can prevent or reverse allograft dysfunction.
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Kidney Transplant I: Introduction
Kidney Transplant II: Surgical Procedure
Kidney Transplant III: Nursing Management
Acute Kidney Injury II: Pathophysiology
Chronic Kidney Disease II: Clinical Manifestations
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