Abstract

A 37-year-old man was referred to the nephrology station due to hypoalbuminaemia = 0.8 g/dL, and generalized oedema including ascite, dyspnoea and creatinine = 1.7 mg/dL. He had been some weeks on a high dose of furosemide without response. On admission, a dipstick revealed no proteinuria and the urinary sediment phase contrast microscopy revealed innumerable crystal casts containing typical oval appearance [1] of the calcium oxalate monohydrate and epithelial cells with crystal inclusions (Figure ​(Figure1A).1A). The anamnesis revealed that 6 months before, the patient had an incarcerated umbilical hernia and intestinal resection. Instead of nephrotic syndrome, we have made a hypothesis of secondary hyperoxaluria due to intestinal insufficiency. One week after stopping diuretics, combining intravenous albumin and alkali therapy, a profuse diuresis occurred with innumerable particles of free forms of calcium oxalate including the bihydrate ones (Figure ​(Figure1B),1B), and with recovery of renal function, we have referred the patient to associated gastroenterological specialized care. Fig. 1 Consecutive fields of the urinary sediment. (A) At patient admission, innumerable crystal casts containing a typical ovoidal appearance of monohydrated calcium oxalate crystals (short arrow) and epithelial cells with crystal inclusions. (B) One week later, ...

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