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Kidney Week

Abstract: PO0045

A Case of Oxalate Nephropathy in the Setting of Clostridium difficile Infection

Session Information

Category: Trainee Case Report

  • 101 AKI: Epidemiology, Risk Factors, and Prevention


  • Chalicheemala, Yasolatha, University Hospitals Cleveland Medical Center Department of Orthopaedics, Cleveland, Ohio, United States
  • Desai, Niraj, Louis Stokes VA Medical Center, Cleveland, Ohio, United States
  • Balabhadrapatruni, Krishna P., Louis Stokes VA Medical Center, Cleveland, Ohio, United States

While hyperoxaluria is a known complication of inflammatory bowel diseases, it is rarely associated with infectious forms of colitis. We report a case of oxalate nephropathy in the setting of Clostridium difficile colitis in a patient with high dietary oxalate ingestion.

Case Description

A 73 year-old black male with stage 3 CKD, diabetes mellitus, hypertension, and hyperlipidemia presented with a 2-week history of intractable diarrhea after finishing a course of oral antibiotics prescribed for acute diverticulitis. Laboratory data showed serum creatinine 15.4 mg/dL, blood urea nitrogen (BUN) 107 m/dL, potassium 8.7 meq/L, total CO2 8 mmol/L . Urinalysis was unremarkable. Imaging showed no renal obstruction. Stool sample tested positive for C difficile. Emergent dialysis was initiated for hyperkalemia. Despite adequate supportive measures, the patient remained oliguric and dialysis dependent. A kidney biopsy, on day 5, showed extensive tubular deposition of calcium oxalate crystals, and moderate to severe tubulointerstitial fibrosis. Further inquiry elicited dietary intake of 1-2 cups of peanuts daily. 24-hr urine collection showed no hyperoxaluria (urine oxalate 24 mg/24h; ref range: 7-44). The patient remains dialysis dependent.


Acute oxalate nephropathy in the setting of Clostridium difficile colitis is rarely reported. The hypothesized etiopathogenesis likely relates to altered gut microbiome, specifically decreased Oxalobacter formigenes, leading to impaired oxalate degradation, increased oxalate absorption, , and subsequent hyperoxaluria (potentially transient) leading to calcium oxalate deposition in the kidneys and AKI. Treatment is mainly supportive. For acute kidney injury in the setting of acute or chronic diarrhea illness, oxalate nephropathy should be considered. Recovery rates are low, with over 50% of patients remaining dialysis dependent.

Calcium oxalate crystals in tubules (PAS stain, polarized light)