Abstract

Recurrent calcium-containing renal calculi are a common and poorly understood problem. Thiazide diuretics decrease urinary calcium excretion but their effect on other parameters of calcium metabolism is not established. The purpose of this study was to determine the effect of chronic administration of thiazide diuretics on intestinal calcium absorption, skeletal calcium turnover, and urinary calcium excretion, and to use this information to attempt to clarify the pathogenesis of idiopathic hypercalciuria. Forty-one patients with recurrent calcium-containing renal calculi were studied; 73% had hypercalciuria, 44% had increased intestinal absorption, and 7% had increased bone turnover. Thiazide diuretics given to 22 patients for 3–16 mo resulted in a consistent reduction in urinary calcium excretion, while calcium absorption was unchanged (< 6%) in 12 patients and significantly decreased (by 20%) in ten patients. Decreased intestinal absorption appeared to be a secondary effect of thiazides, presumably due to reduced urinary calcium losses. Bone turnover was significantly decreased by thiazides in each case in which it had been elevated and was unchanged in patients with initially normal values. These results indicate that increased bone turnover is probably not the primary defect in idiopathic hypercalciuria. The effects of long-term thiazide diuretic therapy on intestinal calcium absorption suggest that there may be two different subpopulations of patients with hypercalciuria, one with primary intestinal hyperabsorption which persists despite correction of urinary losses, and one with primary renal loss of calcium.

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