Abstract: SA-PO0328
From Nephrolithiasis to Oxalate Nephropathy with Dialysis Dependence: Kidney Biopsy Still Rules
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
- Obimdike, Faith, Medical University of South Carolina, Charleston, South Carolina, United States
- Fulop, Tibor, Medical University of South Carolina, Charleston, South Carolina, United States
- McMahon, Blaithin A., Medical University of South Carolina, Charleston, South Carolina, United States
- Caballero, Corynne M., Medical University of South Carolina, Charleston, South Carolina, United States
Introduction
Oxalate nephropathy is an underrecognized cause of progressive chronic kidney injury.
Case Description
A 63-year-old male with a history of monoclonal gammopathy of undetermined significance, calcium oxalate nephrolithiasis, insulin-dependent type 2 diabetes, hypertension and chronic kidney disease 3b presented with nausea, vomiting, and severe acute kidney injury. Baseline seCr was 1.9 mg/dL, with a current rise to 12.5 mg/dL. Urinalysis showed large blood and 21–50 red blood cells and 11–20 white blood cells per high-power field and a microalbumin-to-creatinine ratio 104.9 mg/g. ANA was 1:80 and kappa/lambda ratio was 1.52. Plasma oxalate was 8.2 µmol/L (normal ≤2 µmol/L). Haptoglobin, PR3, MPO, complement (C3,C4), anti-GBM antibodies, syphilis, HIV, rheumatoid factor, and hepatitis B and C serologies were unremarkable. Ultrasound showed kidneys measuring 12.9 cm (left) and 11.1 cm (right), with increased bilateral cortical echogenicity. Kidney biopsy showed severe acute tubular injury with calcium oxalate deposition and severe interstitial fibrosis and tubular atrophy with marked fibrointimal thickening. Staining for kappa and lambda light chains was equally distributed in the tubulo-interstitium. Despite dialysis and calcium carbonate supplementation, the patient remained dialysis-dependent at two months.
Discussion
This case highlights important considerations. Firstly, serum oxalate level may complement serologic work-up. Second, in the presence of a competing hypothesis such as monoclonal gammopathy or diabetic process, kidney biopsy remains essential. Finally, the existing diagnosis of nephrolithiasis should focus attention on the possibility of oxalate nephropathy contributing to accelerated disease progression.
H&E-stained sections demonstrate numerous colorless, fan-shaped crystals compatible with calcium oxalate. Crystals are identified within tubular lumens as well as within the tubular epithelial cells and are associated with widespread tubular injury with epithelial flattening and scattered chronic interstitial inflammation. Under polarized light, the crystals are strongly refractile and more readily apparent.