Urinary Excretion of Prostaglandin F2α and 6-Keto-Prostaglandin F1αa during Volume Expansion in Patients with Glomerulonephritis

Abstract

Patients (13) with active IgA glomerulonephritis (IgA GN), ten patients with a history of Henoch-Schoenlein glomerulonephritis (HS GN) and 9 healthy controls were studied during hydropenia (HP) and 3% volume expansion (VE) with isotonic saline. Clearance of inulin and p-aminohippurate, urinary excretion of Na, immunoreactive prostaglandin F2.alpha. (PGF2.alpha.) and 6-keto-prostaglandin F1.alpha. (6-keto-PGF1.alpha.) were determined. The patients with a history of HS GN had normal blood pressure and renal function. As in the controls, the urinary excretion of PGF2.alpha. decreased and the excretion of 6-keto-PGF1.alpha. increased during VE. In the patients with IgA GN the glomerular filtration rate (GFR) was normal, markedly reduced and supernormal. Five patients had hypertension and an increased NA excretion in relation to the GFR during VE. As a group, the patients with IgA GN increased their urinary excretion of 6-keto-PGF1.alpha. during VE, while the excretion of PGF2.alpha. did not change. In relation to the GFR, the urinary excretion of PGF2.alpha. and 6-keto-PGF1.alpha. was markedly increased in 2 patients with low GFR, which implies that these substances play a role in advanced renal disease. VE had little effect on PG excretion in these patients. In the hypertensive patients the urinary excretion of PGF2.alpha. and 6-keto-PGF1.alpha. was the same as in those with normal blood pressure. PG are not likely to mediate the increased natriuretic response to VE in hypertension.