Urinary excretion of prostaglandin F2 alpha and 6-keto-prostaglandin F1 alpha during volume expansion in patients with glomerulonephritis.

Thirteen patients with active IgA glomerulonephritis (IgA GN), ten patients with a history of Henoch-Schönlein glomerulonephritis (HS GN) and nine healthy controls were studied during hydropenia (HP) and 3% volume expansion (VE) with isotonic saline. Clearance of inulin and para-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 PGF 2 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 two 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. PGs are therefore not likely to mediate the increased natriuretic response to VE in hypertension.