“…Recent investigations in several laboratories (1)(2)(3)(4) using an experimental model of acute, proliferative glomerulonephritis in the rat have focused attention on the coupling between single nephron glomerular filtration rate (SNGFR)l and the absolute rate of fluid reab- 1 Abbreviationis uscd in this paper: A/G, albumin/globulin; AP, femoral arterial pressure; APR, absolute rate of fluid reabsorption by the renal proximal tubule; C, protein concentration; CA, CE, afferent and efferent C, respectively; CL, hilar lymph protein concentration; FF, filtration fraction; GBM, glomerular basement membrane; Kr, ultrafiltration coefficient; Kr, reabsorption coefficient; NSN, nephrotoxic serum nephritis; AP, transcapillary hydraulic pressure difference; PC, PE, PGC, PT, hydraulic pressure in peritubular capillaries, efferent arterioles, glomerular capillaries, and proximal tubules, respectively; Pr, net driving force of reabsorption; P1>, driving pressure for ultrafiltration; PUFA, PUFE, net PUF at the afferent and efferent ends, respectively, of the glomerular capillary; 7r, colloid osmotic pressure; Air, transcapillary osmotic pressure difference; sorption by the renal proximal tubule (APR) in this disorder. In each study it was observed that as filtration rate was reduced, the absolute rate of fluid reabsorption to the end of the proximal convoluted tubule was likewise reduced, although not always in proportion to the reduction in SNGFR.…”