Abstract

o the Editor: We have 2 questions for Dr Beyea, who described a atient with acute phosphate nephropathy after consumption f oral sodium phosphate solution (OSPS) for colonoscopy. heir report belongs to a small group of recently published ases describing coincidence of acute renal failure after owel cleansing with OSPS and renal heavy deposition of alcium phosphate concretions. First, the authors wrote that phosphate nephropathy difers from nephrocalcinosis by virtue of “distinct histopathoogic findings.” We question the accuracy of the distinction etween nephrocalcinosis and phosphate nephropathy. ephrocalcinosis refers to intrarenal deposits of calcium, egardless of whether these deposits occur in the form of hosphate or oxalate salts. In our view, phosphate nephropahy represents an acute nephrocalcinosis. Second, the authors wrote that the patient “has required anagement for anemia and secondary hyperparathyroidsm,” but they did not mention the time of follow-up of the hronic renal disease. Is there any possibility that the paient’s hyperparathyroidism was primary? Underlying sublinical primary hyperthyroidism might be a very appealing actor to explain the intriguing puzzle of why only very few atients develop this ominous complication among all the eople using OSPS. Primary hyperparathyroidism has been escribed in one case and occurred in another case we have bserved (unpublished), is present in greater than 1% of eople, may be undiagnosed when acute hyperphoshatemia lowers serum calcium levels, and offers the best onditions for nephrocalcinosis in the presence of an oral harge of phosphate, as it is demonstrated in experimental ettings. Piero Stratta, MD Sara Barbieri, MD Elisa Lazzarich, MD Roberta Fenoglio, MD Marco Quaglia, MD Departments of Clinical and Experimental Medicine, Nephrology and Transplantation, and International Research Center Autoimmune Diseases (IRCAD) Renal Care Unit San Lazzaro Hospital Alba, Italy

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