The Influence of Renal Prostaglandins on Urinary Calcium Excretion in Idiopathic Urolithiasis

Publisher Website
Google Scholar
Abstract
Hypercalciuria is well recognized as an important factor in the cause of idiopathic Ca stone disease. Identification of the exact mechanisms for the renal tubular handling of Ca has proved elusive; treatment methods to alter the concentration of urine Ca in hypercalciuric stone formers were nonspecific. Renal prostaglandins [PG] influence intrarenal hemodynamics and tubular electrolyte excretion. As the renal handling of Na and Ca is intimately related, the possibility that the mechanism underlying hypercalciuria may be PG mediated was considered. Experiments were performed in conscious Sprague-Dawley rats (n = 10) to determine the change in Ca excretion following PG synthetase inhibition with indomethacin. Ca excretion was significantly reduced (P < 0.01), compared with control animals (n = 10). Further experiments were performed in anesthetized monkeys (Macaca fascicularis) to see if the inhibitory effect of indomethacin was reversible. Exogenous prostaglandin (PGE2) infusion resulted in a marked calciuretic response without producing changes in glomerular filtration rate or blood pressure. Hypercalciuric patients (43) were treated with a PG inhibitor for periods ranging from 2 to 4 wk and all showed a significant fall in urinary Ca excretion to within the normal range. Apparently, PGE2 is a hormone which determines the renal handling of Ca by influencing renal tubular function.