Abstract: SA-PO0326
A Hidden Cause of Oxalate Nephropathy: Pancreatic Neuroendocrine Tumor-Induced Exocrine Insufficiency
Session Information
- AKI: Case Reports - Drug/Toxin Injury, Crystals, Obstruction, and Unusual Presentations
October 24, 2026 | Location: Exhibit Hall A, Convention Center
Abstract Time: 10:00 AM - 12:00 PM
Category: Acute Kidney Injury
- 102 AKI: Clinical, Outcomes, and Trials
Authors
- Kaur, Harpreet, UC Davis Health, Sacramento, California, United States
- Gupta, Rajib K., UC Davis Health, Sacramento, California, United States
- Kapa, Nandakishor, UC Davis Health, Sacramento, California, United States
Introduction
Pancreatic exocrine insufficiency is a recognized but underappreciated cause of enteric hyperoxaluria and oxalate nephropathy. Oxalate nephropathy is commonly associated with bariatric surgery, inflammatory bowel disease, and chronic pancreatitis. We present a case of oxalate nephropathy secondary to pancreatic duct obstruction from a pancreatic neuroendocrine tumor (pNET).
Case Description
A 70-year-old male with type 2 diabetes mellitus, hypertension, CKD stage IIIa with albuminuria, and a pancreatic head neuroendocrine tumor causing marked pancreatic duct dilation presented with one week of nausea, vomiting, and diarrhea. Laboratory evaluation revealed severe acute kidney injury, with serum creatinine of 7.57 mg/dL from a baseline of 1.7 mg/dL several months earlier. Proteinuria also worsened from approximately 500 mg/day to 3 g/day during hospitalization. Urine microscopy was negative for dysmorphic red blood cells, and renal ultrasound showed no obstruction. Given the rapid decline in kidney function and concern for alternative etiologies, including IgG4-related kidney disease, a native kidney biopsy was performed. Biopsy showed glomerulosclerosis with diffuse and nodular mesangial expansion, along with patchy acute tubular injury and numerous intratubular oxalate crystals, consistent with oxalate nephropathy.
Discussion
The patient’s oxalate nephropathy was likely secondary to pancreatic exocrine insufficiency from chronic pancreatic duct obstruction caused by the pNET. Marked ductal dilation likely reflected pancreatic parenchymal atrophy with impaired exocrine function. Fecal elastase was 146 µg/g, consistent with pancreatic insufficiency. Fat malabsorption increases free oxalate absorption, causing enteric hyperoxaluria. Excess oxalate is filtered by the kidneys, where calcium oxalate crystal deposition leads to tubular injury and interstitial inflammation. Early recognition is important, as oxalate nephropathy often presents with rapidly progressive acute kidney injury and may result in irreversible kidney failure.