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Abstract: TH-PO842

Enteric Hyperoxaluria With Recurrent Oxalate Nephropathy

Session Information

Category: Health Maintenance‚ Nutrition‚ and Metabolism

  • 1400 Health Maintenance‚ Nutrition‚ and Metabolism


  • Sheth, Himesh, Brown University Warren Alpert Medical School, Providence, Rhode Island, United States
  • Yu, Tammy, Brown University Warren Alpert Medical School, Providence, Rhode Island, United States
  • Tang, Jie, Brown University Warren Alpert Medical School, Providence, Rhode Island, United States

Enteric hyperoxaluria (EH) can lead to acute kidney injury (AKI), end-stage renal disease (ESRD) and represents therapeutic challenge. Here we present a case of recurrent oxalate nephropathy in a kidney transplant recipient, illustrating the potential aggressive nature of EH and the challenges in treating this condition

Case Description

77-year-old Caucasian lady with hypertension, diabetes, and obesity, developed AKI three years after her Roux-en-Y gastric bypass, with serum creatinine (sCr) rose to of 7 mg/dl from a baseline of 0.7 mg/dl. Kidney biopsy at the time showed extensive tubular injury with numerous calcium oxalate (CaO) inclusions superimposed on moderate interstitial fibrosis and tubular atrophy. Patient ultimately started on hemodialysis four months later and underwent living unrelated kidney transplant 12 months after the onset of AKI, with sCr improved to 0.7 mg/dl. However, six months later, patient developed AKI again following a bout of diarrhea, sCr rose to 3 mg/dl with urine sediment showing features of tubular injury. Due to concern for graft rejection, patient underwent allograft biopsy which again showed intratubular CaO inclusions without signs of rejection. 24-hour urine collection revealed an elevated oxalate level (62 mg), low citric acid (<20mg) pH of 5.1, urine calcium of 70 mg. Her diarrhea resolved after the adjustment of her immunosuppressive regimen. But AKI persisted with 24hr urine oxalate unexpectedly worsened to 92 mg. Patient was then started on potassium citrate (KC) to alkalize urine and to prevent CaO crystallization, Calcium carbonate with meals to reduce oxalate absorption from the gastrointestinal tract in addition to dietary oxalate restriction. She responded well initially, sCr improved to 1.37 mg/dl, along with a reduction in 24-hour urine oxalate and rises in urine citric acid and pH (7.1). Unfortunately, sCr worsened again to 1.7 mg/dl 6 weeks later. Iatrogenic milk alkali syndrome was suspected. Calcium carbonate was stopped, and patient continued dietary oxalate restriction and KC supplementation. Her sCr improved again to 1.3 mg/dl 4 months later and repeat 24-hour urine showed oxalate 55 mg, citric acid 102 mg, Ca <20 mg, pH 5.55.


Enteric oxalate nephropathy is often under recognized, and, if left untreated, can lead to ESRD and allograft injury. Current treatment options are limited although several promising medications are on the horizon.