Altered glomerular permselectivity to neutral dextrans and heteroporous membrane modeling in human pregnancy.

Hyperfiltration precedes renal function loss in several nephropathies. Animal studies suggest this may be due to accompanying increases in transglomerular capillary hydrostatic pressure difference (delta P) and/or altered glomerular processing of macromolecules. Renal hemodynamics increase strikingly in human pregnancy. To test the hypothesis that these alterations are not potentially harmful, clearances of inulin, p-aminohippurate, and neutral dextrans were measured at 16- and 36-wk gestation, then 4 mo postpartum, in 11 normotensive women. Results were analyzed using two computer modeling programs. Glomerular filtration rate and renal plasma flow (RPF) were markedly elevated in early and late pregnancy (135 +/- 6 and 895 +/- 53 and 135 +/- 6 and 754 +/- 32 ml/min, respectively, vs. 87 +/- 7 and 520 +/- 17 ml/min postpartum). Gestational hyperfiltration was primarily due to RPF increments with a minor contribution from decrements in capillary oncotic pressure. Fractional dextran clearances (particularly the smaller dextrans, 30-39 A radii) were lower in early pregnancy, decreasing further in late pregnancy. There was no evidence of increased delta P and alterations in glomerular membrane porosity resolved postpartum. These data provide a database by which to study effects of pregnancy on chronic renal disease.