Title: A Case of Oxalate Nephropathy Due To Excessive Black Tea Consumption

Author(s): Celeste Charchenko, MD; Erdal Sarac, MD; Hilmer Negrete, MD; Denis Lunne, MD

Email: CCharchenko@mercy.com

Introduction: Whether endogenously produced or ingested, oxalate is primarily excreted renally. When hyperoxaluria occurs, acutely or a chronically mild supersaturation, the likelihood of deposition in renal tissue increases. We present a case of biopsy-confirmed oxalate nephropathy due to excessive consumption of black tea.

Case: A 64-year-old Caucasian male was brought to the emergency department in December 2023 by his caregiver with altered mental status, weakness, fatigue, and poor oral intake. The caregiver stated the patient had been sleeping up to 20 hours daily and estimated it had been 24-48 hours since he had last urinated.  Initial laboratory tests revealed creatinine (Cr) 7.0mg/dL, a drastic increase from his baseline Cr 0.7mg/dL on chart review. Urinalysis was negative for hematuria, proteinuria, or pyuria. No evidence of hydronephrosis or obstructing calculi was found on imaging. The prostate was not enlarged and the bladder appeared normal with a volume of 378mL.  Due to the rapid progressive renal failure with essentially negative renal imaging, renal replacement therapy was initiated and kidney biopsy obtained. The pathology report was consistent with oxalate nephropathy noting numerous calcium oxalate crystals and marked tubular injury.  As mentation improved with renal replacement therapy, further questioning revealed the patient was drinking two or more liters of black tea daily. He had no prior history of renal dysfunction, kidney stones, family history of kidney disease, ethylene glycol ingestion, chronic pancreatitis, gastric bypass, bowel resection, or malabsorption condition.

A total of six dialysis sessions were completed by mid-January 2024 before the patient decided to forego further renal replacement treatment. At discharge, Cr level was 2.1mg/dL with fluctuating but improved urine output. Approximately one month later, Cr had further decreased to 1.81mg/dL.

Conclusion: There are few biopsy-confirmed cases of oxalate nephropathy secondary to oxalate-rich diets. Our case highlights a rarely reported but potentially devastating cause of renal injury and the importance of obtaining a thorough history leading to prompt treatment and prevention of further calcium oxalate deposition.