ASN's Mission

ASN leads the fight to prevent, treat, and cure kidney diseases throughout the world by educating health professionals and scientists, advancing research and innovation, communicating new knowledge, and advocating for the highest quality care for patients.

learn more

Contact ASN

1401 H St, NW, Ste 900, Washington, DC 20005

email@asn-online.org

202-640-4660

The Latest on Twitter

Kidney Week

Abstract: PO0191

Crystal Clear: A Case of Oxalate Nephropathy

Session Information

  • AKI Mechanisms - 2
    October 22, 2020 | Location: On-Demand
    Abstract Time: 10:00 AM - 12:00 PM

Category: Trainee Case Report

  • 103 AKI: Mechanisms

Authors

  • Jones, Deanna Nicole, Wake Forest University, Winston-Salem, North Carolina, United States
  • Pirkle, James L., Wake Forest University, Winston-Salem, North Carolina, United States
Introduction

Oxalate nephropathy is an uncommon and potentially devastating cause of acute kidney injury that can lead to end-stage kidney disease. Oxalate nephropathy can be hereditary (as in hereditary hyperoxaluria), related to toxins (such as ethylene glycol), medications, like high-dose vitamin C, or enteric malabsorption (such as gastric bypass surgery or malabsorptive disorders). Oxalate nephropathy occurs when calcium oxalate crystals form and deposit in the renal tubules and interstitium, leading to acute tubular necrosis.

Case Description

A 71 year old female with a medical history of pancreatic adenocarcinoma s/p Whipple procedure seven months earlier and chronic kidney disease stage 3 (baseline creatinine 1.0 mg/dL) presented to the hospital with elevated serum creatinine found incidentally on outpatient labs. Initial evaluation was concerning for volume depletion, as she improved with intravenous fluids. Over the next several months, she had repeated hospital admissions with worsening non-oliguric renal failure that seemed to respond to intravenous fluids in the hospital but worsened at outpatient visits. Urinalysis repeatedly showed no microscopic hematuria and low-level proteinuria, and urine microscopy showed coarse granular casts, consistent with acute tubular necrosis. Kidney biopsy was consistent with acute tubular injury and extensive tubular calcium oxalate deposition concerning for oxalate nephropathy.

Discussion

Oxalate nephropathy is a rare complication of pancreatic surgery and ascorbic acid use. Vitamin C is metabolized to oxalate and then excreted in the urine. In malabsorptive disorders, a higher concentration of fatty acids are present in the gastrointestinal tract, which bind calcium, leaving less to bind oxalate, and thus more oxalate is absorbed. High urinary oxalate can cause crystallization in tubules, leading to acute renal failure. Treatment is supportive, with removal of offending agents, oral calcium supplementation, and adequate oral hydration. Despite this, our patient progressed to end-stage renal disease requiring dialysis.