Lack of effect of prostaglandin inhibition on calcium excretion in normal volunteers.
Recent data have shown that administration of indomethacin to patients with hypercalciuric nephrolithiasis decreased urinary calcium excretion, implying a possible pathogenic role for renal prostaglandins in hypercalciuria. To explore this hypothesis we administered indomethacin, ketoprofen and aspirin to normal volunteers for 6 days and assessed daily creatinine clearance and urinary excretion of sodium and calcium. In contrast to previous studies, subjects were maintained on a constant metabolic diet. These nonsteroidal anti-inflammatory drugs decreased urinary sodium excretion but had no effect on creatinine clearance or urinary calcium excretion. In summary, our data do not support an important physiologic role of renal prostaglandins in renal calcium excretion in normal subjects.
D000328:Adult; D001241:Aspirin / Q000494:pharmacology; D002118:Calcium / Q000652:urine*; D003404:Creatinine / Q000652:urine; D006801:Humans; D007213:Indomethacin / Q000494:pharmacology; D007660:Ketoprofen / Q000494:pharmacology; D008297:Male; D011448:Prostaglandin Antagonists / Q000494:pharmacology*; D012964:Sodium / Q000652:urine
D011448:Prostaglandin Antagonists; D007660:Ketoprofen; D012964:Sodium; D003404:Creatinine; D001241:Aspirin; D002118:Calcium; D007213:Indomethacin