Hypercalciuria probably accounts for the majority of renal stones recovered from patients in the United States.1 Knowledge of the pathophysiologic mechanisms responsible for hypercalciuria has increased dramatically with advances in our understanding of the regulation of calcium and vitamin D metabolism. Depending on dietary calcium intake, approximately one third to one half of ingested calcium is absorbed. The absorbed calcium is distributed in the extracellular fluid. Exchanges occur between the extracellular pool, intracellular pool, and bone. Calcium is lost from the body in urine and in the gut, but the rate of loss of calcium approximates the rate of entry, and thus balance is maintained. Hence, the control of this balance resides in regulation of intestinal absorption and urinary excretion.
Intestinal absorption is regulated by 1,25-dihydroxyvitamin D (1,25-[OH]2D), the most potent metabolite of vitamin D; 1,25-(OH)2D is the product of the 1-hydroxylation of 25-hydroxyvitamin D,