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Letter to the Editor
ARTICLE IN PRESS
doi:
10.25259/IJN_699_2025

Acute Oxalate Nephropathy Following Omission of Pancreatic Enzyme Therapy

Department of Nephrology, Venkateshwar Hospital, New Delhi, India
Department of Pathology, BLK-MAX, Super Speciality Hospital, New Delhi, India

Corresponding author: Prem P Varma, Department of Nephrology, Venkateshwar Hospital, New Delhi, India. E-mail: varmapp123@rediffmail.com

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This is an open access journal, and articles are distributed under the terms of the Creative Commons Attribution-NonCommercial-ShareAlike 4.0 License, which allows others to remix, transform, and build upon the work non-commercially, as long as appropriate credit is given and the new creations are licensed under the identical terms.

How to cite this article: Varma PP, Soni A, Duggal R. Acute Oxalate Nephropathy Following Omission of Pancreatic Enzyme Therapy. Indian J Nephrol. doi: 10.25259/IJN_699_2025

Dear Editor,

A 40-year-old male with chronic kidney disease (serum creatinine: 2 mg/dL) presented with weakness and rapidly progressive renal failure (serum creatinine: 6.24 mg/dL).

Kidney biopsy revealed normal glomeruli and classic features of acute oxalate nephropathy (AON). The tubules and interstitium were infiltrated with oxalate crystals with surrounding inflammation and tubular atrophy. The crystals showed positive birefringence under polarized light, and interstitial fibrosis and tubular atrophy was 30-35% [Figure 1].

(a) Section shows oxalate crystals in the tubules (black rectangle) and a focal giant cell reaction to the crystals (arrow) [Hematoxylin and Eosin (H&E) stain, original magnification x400]. (b) The crystals exhibit strong birefringence under polarized light (H&E stain, under polarized light, original magnification x400).
Figure 1:
(a) Section shows oxalate crystals in the tubules (black rectangle) and a focal giant cell reaction to the crystals (arrow) [Hematoxylin and Eosin (H&E) stain, original magnification x400]. (b) The crystals exhibit strong birefringence under polarized light (H&E stain, under polarized light, original magnification x400).

A detailed history revealed that the patient suffered from acute necrotizing pancreatitis in January 2024. He had been non-compliant with his pancreatic enzyme replacement therapy (PERT) since February 2025. Diagnostic workup confirmed elevated urinary oxalate (41.4 mg/day), low stool elastase (<27.1 µg/g), and chronic pancreatitis on CT abdomen. Patient was managed with intravenous fluids, pyridoxine, low oxalate, high calcium diet, and resumption of PERT. Renal function showed partial improvement, with serum creatinine stabilizing at 4.7 mg/dL.

AON diagnosis is based on three criteria: (i) rapidly progressive renal failure, (ii) presence of oxalate crystals in tubules, and (iii) exclusion of other causes of AKI. In the setting of chronic pancreatitis, dietary calcium, which typically binds with oxalate and prevents its absorption, instead binds with unabsorbed fats, leaving oxalate to be absorbed into the bloodstream, resulting in hyperoxalemia and AON. Diagnosing chronic pancreatitis-related AON involves confirmation of pancreatic insufficiency (fecal elastase excretion <200 μg/g, steatorrhea >6 g/d or pancreatic imaging). AON is a rare, often overlooked, but severe complication of chronic pancreatitis with a poor outcome; >50% of patients become dialysis dependent within a month.1-3

This case emphasizes that chronic pancreatitis can result in irreversible renal failure and stresses the importance of regular PERT.

Conflicts of interest

There are no conflicts of interest.

References

  1. , , , , , . Oxalate nephropathy: A review. Clin Kidney J. 2021;15:194-20.
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  2. , , , , , . Etiologies, clinical features, and outcome of oxalate nephropathy. Kidney Int Rep. 2020;5:1503-9.
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  3. , , , , , , et al. Hidden in plain sight: An unusual cause of rapidly progressive renal failure. IJN. 2018;28:240-43.
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