The influence of indomethacin and possible role of prostaglandins on calcium renal excretion.

Our aim was to evaluate the possible role of prostaglandins (PG) on renal calcium excretion in humans through the PG inhibitory effects of indomethacin. Renal calcium excretion was evaluated by a technique of impulse analysis which gives a function W(t) specific of the tubular calcium transport. Several parameters were derived from this function: (1) the fractional excretion of filtered calcium as % of total dose (FECa % TD); (2) the peak excretion rate, and (3) the mean transit time (MTT, min). The aforementioned parameters were determined in 7 healthy subjects in basal conditions and again after 10 days of treatment with 100 mg indomethacin daily. FECa was significantly (p less than 0.02) higher with indomethacin (8.18 +/- 0.97) than under basal conditions (5.02 +/- 0.57). The peak excretion rate and MTT remained unchanged after indomethacin. These results indicate that indomethacin increases renal calcium excretion. As indomethacin did not produce any significant change in glomerular filtration rate (125 +/- 7 ml/min before vs. 129 +/- 9 ml/min after) one can assume that PG play a role in tubular calcium reabsorption. However, the mechanism remains to be elucidated: direct action or mediated through the cyclic AMP system.