Response to Exogenous 1,25(OH)₂D during a Low-Calcium Diet in Normal Subjects and Idiopathic Renal-Stone Formers

Abstract

A significant number of patients who develop renal stones have evidence of hypercalciuria. It is generally agreed that this increase in urinary calcium excretion is one of the risk factors favoring calcium-oxalate supersaturation, calcium salt precipitation, and stone growth. The mechanisms responsible for the hypercalciuria may involve intestinal calcium absorption, renal-tubular calcium reabsorption, and the regulation of bone mineral content. With the idea of further clarifying the possible pathogenetic mechanisms related to the hypercalciuria, we designed a prospective protocol where we studied normal subjects and a group of renal stone formers before and after the administration of oral 1,25(OH)₂D₃ (1,25-D). Our results suggest that hypercalciuric renal-stone formers do not have increased sensitivity to exogenous 1,25-D and that other factors besides 1,25-D could be involved in the pathogenesis of hypercalciuria.