Role of prostaglandins in protein-induced glomerular hyperfiltration in normal humans.

In six healthy male volunteers we studied the effect of indomethacin on the renal hemodynamic adaptations to an acute oral protein load. Control and protein loading studies without and with indomethacin were performed under sustained water diuresis. In the control studies without indomethacin, creatinine (CCr) and inulin clearance (CIn) remained stable and p-aminohippurate (PAH) clearance (CPAH) and kaliuresis slightly decreased while natriuresis progressively increased. Urinary prostaglandin E2 (PGE2) excretion remained stable. Indomethacin had no effect on these control values except on natriuresis and PGE2 excretion. After protein loading CCr, CIn, and CPAH progressively increased to reach a peak 2 h after protein intake. Natriuresis, kaliuresis, and urinary PGE2 excretion also increased significantly. After indomethacin the peak increase of CCr, CIn, and CPAH during the 2nd h was significantly blunted. Indomethacin had no effect on the increased sodium and potassium excretion. The increase of PGE2 excretion was significantly attenuated by indomethacin. The results presented suggest that renal prostaglandins play at least a partial role in the renal hemodynamic adaptations to protein loading.