Maddox D A, Bennett C M, Deen W M, Glassock R J, Knutson D, Daugharty T M, Brenner B M
J Clin Invest. 1975 Feb;55(2):305-18. doi: 10.1172/JCI107934.
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.
在22只处于肾毒性血清性肾炎（NSN）自体早期阶段的Wistar大鼠的浅表性肾小球毛细血管、出球小动脉和近端小管中测量了压力和流量。通过免疫荧光显微镜在肾小球毛细血管壁中证实了兔和大鼠IgG以及补体C3成分的线性沉积。光学显微镜显示弥漫性增殖性肾小球肾炎，且存在蛋白尿。尽管NSN大鼠的全肾和单肾肾小球滤过率（GFR）（分别为0.8±0.04 SE2 ml/min和2±2 nl/min）与16只体重匹配的正常缺水对照大鼠（0.8±0.08和28±2）的值相比没有变化，但肾小球动力学出现了重要改变。NSN组的平均跨毛细血管液压差（deltaP）平均为41±1 mmHg，而对照组为32±1 mmHg（P＜0.005）。两组肾小球毛细血管入球端（piA）的胶体渗透压相似（16 mmHg），但NSN组出球端（piE）的胶体渗透压升高幅度（至29±1 mmHg）远小于对照组（33±1，P＜0.025）。因此，对照组获得了表示滤过压力平衡的deltaP和piE相等的情况，而NSN大鼠未获得。虽然NSN组的肾小球血浆流速（88±8 nl/min）略高于对照组（76±6，P＞0.2），但NSN大鼠未能达到滤过平衡主要是由于肾小球毛细血管超滤系数Kf显著下降至平均值0.03 nl/（s·mmHg），远低于最近在正常大鼠中发现的值0.08 nl/（s·mmHg）。因此，尽管存在广泛的肾小球损伤，从形态学和低Kf可以证明，但GFR仍保持正常。GFR的维持主要源于deltaP的增加，这倾向于增加滤过的净驱动力，从而补偿Kf的降低。
