A Not-So-Crystal-Clear Case of Oxalate Nephropathy

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.Figure. Kidney biopsy showing oxalate crystals 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

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Publication Details

Journal
Journal of the American Society of Nephrology
Published
2025-10-01
DOI
https://doi.org/10.1681/asn.2025q39aeqj5
Primary Topic
Kidney Stones and Urolithiasis Treatments
Type
article
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article

A Not-So-Crystal-Clear Case of Oxalate Nephropathy

Journal of the American Society of Nephrology
Kidney Stones and Urolithiasis Treatments
article

A Not-So-Crystal-Clear Case of Oxalate Nephropathy

article en

Abstract

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.Figure. Kidney biopsy showing oxalate crystals 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

Journal of the American Society of NephrologyVol. 36(10S)
Pennsylvania Hospital (US)
Good health and well-being
Openalex Percentile: Top 33%
Kidney Stones and Urolithiasis Treatments
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