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Antacid‐induced phosphate depletion syndrome presenting as nephrolithiasis
Author(s) -
Harmelin D. L.,
Martin F. I. R.,
Wark J. D.
Publication year - 1990
Publication title -
australian and new zealand journal of medicine
Language(s) - English
Resource type - Journals
SCImago Journal Rank - 0.596
H-Index - 70
eISSN - 1445-5994
pISSN - 0004-8291
DOI - 10.1111/j.1445-5994.1990.tb00427.x
Subject(s) - antacid , hypercalciuria , medicine , endocrinology , parathyroid hormone , phosphate , phosphate binder , weakness , ingestion , gastroenterology , calcium , kidney disease , surgery , hyperphosphatemia , biochemistry , chemistry
A 29‐year‐old insulin‐dependent diabetic woman developed phosphate depletion, nephrolithiasis and bilateral ureteric obstruction due to antacid abuse. Unlike previous descriptions of chronic phosphate depletion, myalgia, weakness and bone pain were absent. Biochemical features included hypophosphataemia, hypercalciuria, hypophosphaturia, elevated plasma 1,25‐dihydroxyvitamin D and low plasma intact parathyroid hormone. These abnormalities were corrected when antacid ingestion was reduced and phosphate intake supplemented. Wepropose that phosphate depletion secondary to antacid abuse caused 1α‐hydroxylase activation and elevation of the plasma 1,25‐dihydroxyvitamin D level, leading to marked hypercalciuria. Once diagnosed, antacid abuse is a readily reversible cause of hypercalciuria and renal stones. Moreover, antacid‐induced phosphate depletion may present with nephrolithiasis in the absence of musculoskeletal symptoms. This report is intended to draw attention to this important cause of renal stone disease.