Determinants of glomerular filtration in experimental glomerulonephritis in the rat

Abstract

Pressures and flows were measured in surface glomerular capillaries, efferent arterioles, and proximal tubules of 22 Wistar rats in the early autologous phase of nephrotoxic serum nephritis (NSN). Linear deposits of rabbit and rat IgG and C3 component of complement were demonstrated in glomerular capillary walls by immunofluorescence microscopy. Light microscopy revealed diffuse proliferative glomerulonephritis, and proteinuria was present. Although whole kidney and single nephron glomerular filtration rate (GFR) in NSN (0.8 ± 0.04 [SE] ml/min and 27 ± 2 nl/min, respectively) remained unchanged from values in 16 weight matched normal hydropenic control rats (0.8 ± 0.08 and 28 ± 2), important alterations in glomerular dynamics were noted. Mean transcapillary hydraulic pressure difference (ΔP) averaged 41 ± 1 mm Hg in NSN versus 32 ± 1 in controls (P < 0.005). Oncotic pressures at the afferent (πA) end of the glomerular capillary were similar in both groups (16 mm Hg) but increased much less by the efferent end (πE) in NSN (to 29 ± 1 mm Hg) than in controls (33 ± 1, P < 0.025). Hence, equality between ΔP and πE, denoting filtration pressure equilibrium, obtained in control but not in NSN rats. While glomerular plasma flow rate was slightly higher in NSN (88 ± 8 nl/min) than in controls (76 ± 6, P > 0.2), the failure to achieve filtration equilibrium in NSN rats was primarily the consequence of a marked fall in the glomerular capillary ultrafiltration coefficient, Kf, to a mean value of 0.03 nl/(s/mm Hg), considerably lower than that found recently for the normal rat, 0.08 nl/(s/mm Hg). Thus, despite extensive glomerular injury, evidenced morphologically and by the low Kf, GFR remained normal. This maintenance of GFR resulted primarily from increases in ΔP, which tended to increase the net driving force for filtration, and thereby compensate for the reduction of Kf.