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, ...
Talk to us
Join us for a 30 min session where you can share your feedback and ask us any queries you have
Disclaimer: All third-party content on this website/platform is and will remain the property of their respective owners and is provided on "as is" basis without any warranties, express or implied. Use of third-party content does not indicate any affiliation, sponsorship with or endorsement by them. Any references to third-party content is to identify the corresponding services and shall be considered fair use under The CopyrightLaw.