Intrarenal pressure and sodium excretion in hypertension of chronic glomerulonephritis in humans.

The relationship between the fractional excretion of filtered sodium (FENa) and the peritubular capillary physical factors (PCPF) in the hypertension (HT) of chronic glomerulonephritis (GN) was examined in hydropenia (C) and during sustained isotonic saline volume expansion (E; 3% net increase of body weight) in 32 GN patients (16 with HT), and compared with our previous findings in 20 normal individuals (NORM) and 19 patients with essential hypertension (EH). Fourteen GN patients (seven with HT) had a 75% reduction of glomerular filtration rate (GFR), the others (nine with HT) had normal or near normal GFR. The PCPF were estimated from the intrarenal venous (wedged) pressure (IRVP) and the calculated efferent arteriolar protein concentration (EAPC). In C, IRVP correlated to GFR (r = 0.682, p less than 0.001) and (FENa) (r = -0.357, p less than 0.05), but IRVP and EAPC were similar in HT and normotension at comparable levels of GFR. The increase of FENa during E (delta FENa) was exaggerated in all HT groups even at reduced levels of GRF, and could not be related to changes in renal hemodynamics or PCPF. delta FENa correlated with mean arterial pressure in C both in GN (r1 = 0.702, p less than 0.01) and in the combined NORM/EH group (r2 = 0.478, p less than 0.01), with r1 greater than r2 (p less than 0.005). The findings indicate that the pathogenesis of hypertension of chronic glomerulonephritis is independent of changes in the PCPF, and are compatible with the idea that humoral factors are the main mediators of the altered sodium excretion during saline volume expansion in the HT of both chronic GN and EH.