C5b-9 increases albumin permeability of isolated glomeruli in vitro.
C5b-9 increases albumin permeability of isolated glomeruli in vitro.
复制标题
C5b-9 增加体外分离肾小球的白蛋白通透性。
DOI：
10.1038/ki.1994.285
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发表时间：
1994
影响因子：
19.6
通讯作者：
Couser,WG
中科院分区：
文献类型：
--
作者：
Savin,VJ;Johnson,RJ;Couser,WG
C5b-9 increases albumin permeability of isolated glomeruliin vitro. Deposition of antibody and activation of the complement cascade are important in both naturally occurring glomerulonephritis and in experimental models including passive Heymann nephritis. We studied the effect of antibody and complement on albumin permeability of isolated glomeruli to determine the role of the terminal complement components (C5-C9) in mediating the proteinuria in nephritis. Isolated glomeruli were treated with anti-Fx1a (Heymann antibody) and then incubated them with pooled human serum, serum in which complement had been inactivated by heat, or serum deficient in C6 or C7. The albumin reflection coefficient (σalbumin) was calculated from the volumetric response of glomeruli to transcapillary oncotic gradients produced by albumin or high molecular weight neutral dextran (252 kD). Convectional permeability to albumin (Palbumin) was calculated as 1-σalbumin. Albumin permeability of control glomeruli was not different from 0. Albumin permeability was not altered by antibody alone but was increased to 0.65 ± 0.04 when antibody treated glomeruli were incubated for 10 minutes with pooled serum as a source of complement. Heat treatment of serum to inactivate complement prevented the increase in permeability. Incubation for 10 minutes with serum without antibody pretreatment caused a lesser increase in permeability of isolated glomeruli (0.18 ± 0.06). Serum deficient in either C6 or C7 did not cause an increase in albumin permeability of antibody pre-treated glomeruli, but incubation with a combination of these sera (now containing the complete cascade) increased permeability to the same extent as did pooled normal serum (0.58 ± 0.04). We conclude that activation of the terminal complement components is required for the increase in glomerular macromolecular permeability caused by anti-Fx1a and that terminal complement activation is sufficient to alter the permeability independent of complement hemodynamic events or contribution by circulating cells.
