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Kidney Week

Abstract: PO0241

Two Cases of Oxalate Nephropathy: An Uncommon Disease, Often Missed

Session Information

  • AKI Mechanisms - 3
    October 22, 2020 | Location: On-Demand
    Abstract Time: 10:00 AM - 12:00 PM

Category: Trainee Case Report

  • 103 AKI: Mechanisms


  • Schretlen, Claire F., West Virginia University Health Sciences Center, Morgantown, West Virginia, United States
  • Neuman, Michelle, West Virginia University Health Sciences Center, Morgantown, West Virginia, United States
  • Chaudhary, Vishy, West Virginia University Health Sciences Center, Morgantown, West Virginia, United States

Oxalate nephropathy is a state of excess oxalate availability leading to damaging calcium oxalate crystal deposition in the renal tubules and interstitium. It is an uncommon but severe cause of renal damage and leads to dialysis dependence in the majority of patients; thus, diagnostic index of suspicion must be high.

Case Description

Patient A was a 58 year old male with 2 prior renal stones but no history of gastric bypass, IBD, or other malabsorptive state who presented with vomiting, metallic taste, and behavior changes. Serum creatinine (SCr) on admission was 10.2 mg/dL (baseline 1.1 mg/dL). Basic workup including ANCA, ANA, dsDNA, C3, C4, and Hepatitis B and C was unremarkable. A renal biopsy showed severe interstitial fibrosis and tubular atrophy with abundant calcium oxalate crystals, and dialysis was initiated. Dietary history revealed daily consumption of 1,000 mg Vitamin C, salads, and nuts. Genetic testing for primary hyperoxalosis was negative. After 1.5 months he was no longer dialysis-dependent but only attained partial renal recovery (SCr 2.67 mg/dL, eGFR 25).

Patient B was a 68 year old male with no history of renal or GI disease who presented with emesis, weakness, and urinary retention. Admission SCr was 7.7 mg/dL (baseline 1.4 mg/dL). Renal function improved slightly after Foley placement for newly diagnosed BPH, but SCr remained elevated with negative initial AKI workup. Renal biopsy showed oxalate nephropathy. Further history revealed only occasional consumption of nuts with daily servings of tea and polyethylene glycol. Patient B’s genetic testing was also negative. He remains on hemodialysis and has been referred for transplant.


Oxalate nephropathy can result from primary (genetic) or secondary mechanisms. The most common secondary causes include increased intestinal oxalate availability (“enteric” hyperoxaluria) and increased dietary consumption. A basic medical history can reveal risk factors for enteric hyperoxaluria, while a thorough review of diet and supplements is often deferred, delaying the diagnosis. In some cases a single cause is not identified, and instead a combination of dietary and pharmacologic factors are to blame. We present 1 case of oxalate nephropathy most likely caused by high-dose Vitamin C, and another case with a less clear etiology aside from vague dietary and medication factors.