Abstract: SA-PO073
From Marathon to Miracles: Managing Dialysis-Dependent Oxalate Nephropathy with Ethylenediamine Tetra Acetic Acid (EDTA)
Session Information
- AKI: Clinical, Outcomes, and Trials - Management
October 26, 2024 | Location: Exhibit Hall, Convention Center
Abstract Time: 10:00 AM - 12:00 PM
Category: Acute Kidney Injury
- 102 AKI: Clinical, Outcomes, and Trials
Authors
- Varanasi, Paavana, Mayo Clinic Arizona, Scottsdale, Arizona, United States
- Ravi, Srekar N., Mayo Clinic Arizona, Scottsdale, Arizona, United States
- Thomas, Leslie F., Mayo Clinic Arizona, Scottsdale, Arizona, United States
Introduction
Oxalate nephropathy is a rare cause of kidney injury due to oxalate crystal deposition within tubules, causing direct tubular injury and obstruction. Excessive vitamin C intake can cause secondary hyperoxaluria and acute kidney injury (AKI). Early diagnosis and management are crucial to prevent ESRD, but there is no known cure. We present a case of stage 3 AKI due to biopsy-proven oxalate nephropathy requiring dialysis that was successfully treated.
Case Description
A 31-year-old female without known medical problems presented with intractable nausea, vomiting, back pain, and minimal urine output after running a marathon. One week prior, she took 400-600 mg of ibuprofen daily for migraine headaches and oral vitamin C supplements. Immediately following the race, she received a total of 3.5 L of IV fluids and one IV vitamin C infusion at mobile hydration units. Labs showed Cr 8.42 mg/dL, BUN 64 mg/dL, and CK 2400 U/L. Urinalysis had pyuria without hemoglobinuria. On hospital presentation, she was oliguric (200-300cc/day) and renal function continued to worsen despite aggressive IV fluid resuscitation. Dialysis was started on hospital day 3 and a kidney biopsy revealed acute tubular injury with abundant calcium oxalate deposits consistent with oxalate nephropathy. Given limited interstitial fibrosis and tubular atrophy (10-15%), she was trialed on IV EDTA 250 mg infusion for 3 consecutive days. She had increased urine output with each subsequent dose and return of kidney function with discontinuation of dialysis.
Discussion
This case demonstrates a novel treatment for oxalate nephropathy with IV EDTA infusion. The patient's recovery from dialysis-dependence is rare. 24-hour urine studies before and after EDTA showed increased oxalate, presumably from renal excretion of soluble oxalate after calcium chelation with EDTA in the tubules. This underscores the consideration of oxalate nephropathy in AKI patients with high vitamin C intake and suggests a potential therapy for further study.