Abstract: SA-PO0039
Vitamin C-Induced Acute Oxalate Nephropathy
Session Information
- AKI: Novel Patient Populations and Case Reports
November 08, 2025 | Location: Exhibit Hall, Convention Center
Abstract Time: 10:00 AM - 12:00 PM
Category: Acute Kidney Injury
- 101 AKI: Epidemiology, Risk Factors, and Prevention
Authors
- Banerjee, Annesha, Stony Brook University, Stony Brook, New York, United States
- Retnakumar, Parvathy, Stony Brook University, Stony Brook, New York, United States
- Parikh, Rushang, Veterans Affairs Medical Center, Northport, New York, United States
- Weissman, Edward, Veterans Affairs Medical Center, Northport, New York, United States
Introduction
Acute Oxalate Nephropathy (AON) is an underdiagnosed condition that carries a poor prognosis, with previous studies estimating 52% of cases develop into kidney failure within the first month [1]. One unsuspecting source for AON is Vitamin C.
Case Description
A 61-year-old man presented with three days non-bloody emesis and diarrhea. He has a medical history of CKD II, T2DM, and polysubstance use disorder. Admission labs notable for creatinine of 13.3 mg/dL (baseline 1.2 mg/dL). Urinalysis showed 30+ protein. Urine toxicology positive for cocaine. The patient reported using cocaine several times in the week prior to admission.
Renal ultrasound was completed without findings of hydronephrosis. Urine microscopy showed 2-3 dysmorphic red blood cells, several calcium oxalate crystals, and few granular casts. Steroids were started for suspected vasculitis. Infectious and autoimmune serologic workup was negative. A kidney biopsy was performed and showed acute tubular injury with intratubular calcium oxalate crystals. Steroids were discontinued, and the patient was continued on supportive care with IV fluids and phosphate binder. Upon further questioning on the possible source of calcium oxalate, he disclosed that the cocaine used may have been mixed with Vitamin C. He did not require hemodialysis throughout his hospital course. His creatinine improved to 10.4 mg/dl on discharge and 2.3 mg/dl two months post-discharge.
Discussion
This case illustrates several teaching points. One, early diagnosis of AON is critical, and can be done with high clinical suspicion and prompt kidney biopsy. Two, treatment for AON has not yet been standardized. Empiric evidence shows that intravenous fluids, oral calcium supplementation, and correction/cessation of the underlying condition are important starting points [1]. In this case, supportive treatment involved continued IV fluids and counseling on drug use cessation. Three, further studies are needed to understand the true risk factors for calcium oxalate nephropathy. Currently, it appears that diabetes mellitus is an important risk factor as these patients excrete increased amounts of oxalate into the urine at baseline. Additional risk factors include male sex, chronic kidney disease, and increased age (on average 56 - 60 years old +) [7]. Our patient shared these risk factors.