A Biopsy-Proven Case of Acute Oxalate Nephropathy from Longevity Remedies
Journal Title: Biomedical Journal of Scientific & Technical Research (BJSTR) - Year 2019, Vol 19, Issue 3
Abstract
Acute oxalate nephropathy is an uncommon etiology of acute kidney injury caused by deposition of oxalate crystals in the kidneys as a result of hyperoxaluria. We report a case of biopsy-proven acute oxalate nephropathy after excessive consumption of A. bilimbi fruit from Longevity remedies. A 66-year-old man with past medical history of hypertension and type 2 diabetes mellitus presented with generalized edema for 7 days. He noticed that his urine volume was significantly decreased but denied history of foamy urine or gross hematuria. He also denied history of vomiting, diarrhea, difficult urination, fever and recent exposure to nephrotoxic medications. Physical examination revealed a stable vital sign, but his eye lids were puffy and pitting edema was observed on both legs. Initial laboratory investigations revealed BUN of 29 mg/dL, creatinine of 6.2 mg/ dL and normal serum electrolyte. His prior creatinine that was done 4 months ago was 1.4 md/dL. His urinalysis was negative for proteinuria and cells. Ultrasonogram of the kidneys and urinary tract was normal without stone or hydronephrosis. Upon further interview, he admitted that he ate 4-5 A. bilimbi fruits preserved in syrup and 250 ml of their juice per day for the past 10 days as herbal remedies for longevity. Further investigations revealed 24- hour urine volume of 848 mL and 24-hour urine oxalate of 15.77 mg (1.76 mmol). The oxalate concentration of the juice was 483.49 mg/dL (53.72 mmol/dL). We decided to perform percutaneous renal biopsy to evaluate for the definite cause of his acute kidney injury and the renal pathology showed evidence of diffused tubular injury with multiple foci of interlobular calcium oxalate crystals (Figures 1 & 2). During the course of his hospitalization, this patient was restrained from oxalate-containing food and received intravenous fluid. His renal function gradually recovered, and his serum creatinine declined from 6.2 mg/dL to 5.2 mg/dL within 2 weeks and returned to near baseline level (2.3 mg/dL). Since urinary excretion is one the main pathways for eradication of oxalate [1], excessive dietary oxalate intake can trigger renal damage as supersaturated oxalate in the urine and bind with calcium, causing crystallization of oxalate in the renal tubules and interstitium, which lead to inflammation and injury to the kidneys [2,3]. A. bilimbi is another fruit that contains a high amount of oxalate. Previous studies have demonstrated that the concentration of oxalate in A. bilimbi fruit could range from 8.6 to 10.3 g/100 g depends on the ripeness and season [4].
Authors and Affiliations
Sukit Raksasuk, Thatsaphan Srithongkul
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