Abstract: SA-PO0969
A Not-So-Crystal-Clear Case of Oxalate Nephropathy
Session Information
- Pathology: Updates and Insights
November 08, 2025 | Location: Exhibit Hall, Convention Center
Abstract Time: 10:00 AM - 12:00 PM
Category: Pathology and Lab Medicine
- 1800 Pathology and Lab Medicine
Authors
- Barrera Gonzalez, Jaimie, Pennsylvania Hospital, Philadelphia, Pennsylvania, United States
- Kim, Kwon Soo, Pennsylvania Hospital, Philadelphia, Pennsylvania, United States
- Palmer, Matthew, Pennsylvania Hospital, Philadelphia, Pennsylvania, United States
Introduction
Enteric hyperoxaluria (EH) results from decreased serum calcium leaving oxalate available for gastrointestinal (GI) reabsorption. Crohn’s disease, cystic fibrosis, chronic pancreatitis, and gastric bypass surgery are causes of EH.1,2 A rare complication of EH include nephrolithiasis, tubulopathy and renal disease known as oxalate nephropathy (ON).3,4 Below we report a complex case of ON from Roux-en-Y gastric bypass (RYGB).
Case Description
A 52-year-old male with a history of RYGB, hypertension, and diabetes presented with weakness. He was found to have an anuric AKI with a Cr 15 mg/dL from a baseline 1.5 mg/dL, severe metabolic acidosis, and hyperkalemia requiring CRRT. Infectious, autoimmune, and vasculitis workup was negative. He underwent a renal biopsy revealing luminal oxalate crystals and interstitial fibrosis consistent with ON. Plasma oxalate levels were elevated at 15 umol/L. Peritoneal dialysis (PD) was initiated, and shortly after transitioned to hemodialysis (HD). He is being evaluated for a kidney transplant and RYGB reversal is recommended.
Discussion
Our case highlights the complex management and prognosis of ON, especially in transplant planning. Diabetes and hypertension cause kidney disease, however, our patient’s severe renal failure suggested a separate etiology supporting urgent renal biopsy. Despite PD and HD our patient had elevated serum oxalate levels favoring systemic oxalosis. Oxalate crystal deposition can occur in multiple organs, and we hypothesize crystal deposition in the peritoneal membrane may have contributed to PD failure. We raise awareness to prompt workup and biopsy in bariatric patients with an AKI and the potential role of peritoneal oxalate deposition.
Table 1. Urine studies
| Urine dipstick | blood, 100 protein, LE |
| Urine microscopy | RBC 10-20, WBC 50-100 with clumps |
| Urine sediment | WBC, RBC, muddy brown casts |
| Urine electrolytes | K 23.6, Na 65, Cr 61.1 |
Abbreviations: LE: leukocyte esterase, RBC: red blood cell, WBC: white blood cell, K: potassium, Na: sodium, Cr: creatinine
Figure. Kidney biopsy showing oxalate crystals