Peritubular capillary hydrostatic and oncotic forces and their relationship to the renal excretion of sodium (UNaV) were examined in 19 patients with moderate and uncomplicated essential hypertension (HT) and compared with data from 20 normotensive subjects (NT). Observations were made in hydropenia (C) and during sustained isotonic saline volume expansion (E; 3% increase in body weight). The intrarenal venous pressure (IRVP) was used as an index of peritubular capillary hydrostatic pressure, and the efferent arteriolar colloid osmotic pressure (COPeff) was estimated from the arterial COP and the filtration fraction. C values (mean +/- SEM) in HT (and NT) were: arterial pressure (MAP) 110 +/- 3 mm Hg (85 +/- 1, p less than 0.001); glomerular filtration rate (GFR) 122 +/- 4 ml/min/1.73 m2 (128 +/- 3, p greater than 0.05); renal blood flow (RBF) 1172 +/- 38 ml/min/1.73 m2 (1298 +/- 48, p less than 0.05); IRVP 25.0 +/- 1.0 mm Hg (24.8 +/- 0.8, p greater than 0.05); COPeff 33.0 +/- 0.7 mm Hg (31.9 +/- 0.6, p greater than 0.05); and UNaV 140 +/- 13 mumole/min (161 +/- 12, p greater than 0.05). During E, the increase of UNaV in HT was more than double that of NT (p less than 0.001) while IRVP did not change in either group (p greater than 0.05); and COPeff fell by 26% (p less than 0.001) in both groups. GFR and RBF increased by 18% (p less than 0.001) and 19% (p less than 0.001) respectively, in HT, but did not change in NT. MAP remained unchanged in both groups. The results indicate that the peritubular capillary physical factors are normal in established essential hypertension, and that these forces are not involved in the exaggerated natriuretic response to volume expansion in essential hypertension.

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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.

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PubMedDate not supplied

Renal function in patients with unilateral staghorn calculi.

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