Determinants of glomerular filtration in experimental glomerulonephritis in the rat.
Determinants of glomerular filtration in experimental glomerulonephritis in the rat.
复制标题
大鼠实验性肾小球肾炎肾小球滤过的决定因素。
DOI：
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发表时间：
1975
影响因子：
15.9
通讯作者：
B. Brenner
中科院分区：
文献类型：
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作者：
D. A. Maddox;C. Bennett;W. Deen;R. Glassock;D. Knutson;T. Daugharty;B. Brenner
在22只Wistar大鼠自体肾毒性血清肾炎（NSN）早期，测定了肾小球表面毛细血管、输出小动脉和近端小管的压力和流量。免疫荧光显微镜观察到兔和大鼠肾小球毛细血管壁IgG和补体C3成分呈线状沉积。光学显微镜检查显示弥漫性增生性肾小球肾炎，并存在蛋白尿。尽管NSN中的全肾和单个肾单位肾小球滤过率（GFR）（分别为0.8 ± 0.04 SE 2 ml/min和2 ± 2 nl/min）与16只体重匹配的正常肾积水对照大鼠的数值（0.8 ± 0.08和28 ± 2）相比保持不变，但观察到肾小球动力学的重要变化。平均跨毛细血管液压差（deltaP）在NSN中平均为41 ± 1 mm Hg，对照组为32 ± 1 mm Hg（P <0.005）。两组肾小球毛细血管输入端（piA）的血压相似（16 mm /g），但NSN组肾小球毛细血管输出端（piE）的血压升高（29 ± 1 mm Hg）远低于对照组（33 ± 1 mm Hg，P <0.025）。因此，Δ P和piE之间相等，表示在对照大鼠中获得而在NSN大鼠中未获得滤过压平衡。而NSN的肾小球血浆流速略高（88 ± 8 nl/min）（76 ± 6，P> 0.2），NSN大鼠未能达到滤过平衡主要是肾小球毛细血管超滤系数Kf显著下降的结果，平均值为0.03 nl/（s × mm Hg），明显低于最近正常大鼠的0.08 nl/（s × mm Hg）。因此，尽管广泛的肾小球损伤，证明形态学和低Kf，GFR保持正常。GFR的这种维持主要是由于deltaP的增加，这往往会增加过滤的净驱动力，从而补偿Kf的降低。
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 plus or minus 0.04 SE2 ml/min and 2 plus or minus 2 nl/min, respectively) remained unchanged from values in 16 weight-matched NORMAL HYDROPENIC control rats (0.8 plus or minus 0.08 and 28 plus or minus 2), important alterations in glomerular dynamics were noted. Mean transcapillary hydraulic pressure difference (deltaP) averaged 41 plus or minus 1 mm Hg in NSN versus 32 plus or minus 1 in controls (P LESS THAN 0.005). Oncotic pressures at the afferent (piA) end of the glomerular capillary were similar in both groups ( 16 mm /g) but increased much less by the efferent end (piE) in NSN (to 29 plus or minus 1 mm Hg) than in controls (33 plus or minus 1, P less than 0.025). Hence, equality between deltaP and piE, denoting filtration pressure equilibrium, obtained in control but not in NSN rats. While glomerular plasma flow rate was slightly higher in NSN (88 plus or minus 8 nl/min) than in controls (76 plus or minus 6, P greater than 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 times mm Hg), considerably lower than that found recently for the normal rat, 0.08 nl/(s times 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 deltaP, which tended to increase the net driving force for filtration, and thereby compensate for the reduction in Kf.