Oxalate Nephropathy: A Case Report of Acute Kidney Injury Due to Juice Diet

Oxalate nephropathy occurs due to the deposition of calcium oxalate crystals in kidney tubules and/or the interstitium as a part of primary or secondary hyperoxaluria. Secondary oxalate nephropathy can occur even with moderately high doses of ascorbic acid intake under yet unidentified clinical circumstances. Vitamin C, although traditionally considered an antioxidant, leads to the formation of superoxide and subsequent generation of reactive oxidant species at pharmacologic concentrations. Ascorbic acid is partly converted to oxalic acid, which is responsible for deposition and renal tubular injury. We report a case of a diabetic patient with normal kidney function who was put on a juice diet for a week due to upper gastrointestinal bleeding. He developed acute kidney injury due to biopsy-proven oxalate nephropathy requiring dialysis. Though he was lost to follow-up after two weeks on dialysis, he was expected to have only a slow recovery or become dependent on dialysis given his age, comorbidities, and extent of tubular involvement. Hence, caution should be exercised before supplementing vitamin C either in its natural form or as a drug. Risk factors for secondary oxalate nephropathy due to excessive intake of oxalate or its precursor are likely to be age, diabetes, dehydration, and underlying chronic kidney disease. Most of the patients do not have a complete recovery of kidney function, and many become dependent on dialysis.