Lafayette R A, Druzin M, Sibley R, Derby G, Malik T, Huie P, Polhemus C, Deen W M, Myers B D
Department of Medicine, Stanford University Medical Center, Stanford University School of Medicine, California 94305-5114, USA.
Kidney Int. 1998 Oct;54(4):1240-9. doi: 10.1046/j.1523-1755.1998.00097.x.
Pre-eclampsia is characterized by hypertension, proteinuria and edema. Simultaneous studies of kidney function and structure have not been reported. We wished to explore the degree and nature of glomerular dysfunction in pre-eclampsia.
Physiologic techniques were used to estimate glomerular filtration rate (GFR), renal plasma flow and afferent oncotic pressure immediately after delivery in consecutive patients with pre-eclampsia (PET; N = 13). Healthy mothers completing an uncomplicated pregnancy served as functional controls (N = 12). A morphometric analysis of glomeruli obtained by biopsy and mathematical modeling were used to estimate the glomerular ultrafiltration coefficient (Kf). Glomeruli from healthy female kidney transplant donors served as structural controls (N = 8).
The GFR in PET was depressed below the control level, 91 +/- 23 versus 149 +/- 34 ml/min/1.73 m2, respectively (P < 0.0001). In contrast, renal plasma flow and oncotic pressure were similar in the two groups (P = NS). A reduction in the density and size of endothelial fenestrae and subendothelial accumulation of fibrinoid deposits lowered glomerular hydraulic permeability in PET compared to controls, 1.81 versus 2.58 x 10(-9) m/sec/PA. Mesangial cell interposition also curtailed effective filtration surface area. Together, these changes lowered the computed single nephron Kf in PET below control, 4.26 versus 6.78 nl/min x mm Hg, respectively.
The proportionate (approximately 40%) depression of Kf for single nephrons and GFR suggests that hypofiltration in PET does not have a hemodynamic basis, but is a consequence of structural changes that lead to impairment of intrinsic glomerular ultrafiltration capacity.
子痫前期的特征为高血压、蛋白尿和水肿。尚未有关于肾功能和结构的同步研究报道。我们希望探究子痫前期肾小球功能障碍的程度和性质。
采用生理学技术对连续的子痫前期患者（PET；N = 13）产后立即估计肾小球滤过率（GFR）、肾血浆流量和入球小动脉胶体渗透压。完成无并发症妊娠的健康母亲作为功能对照（N = 12）。通过活检获得的肾小球进行形态计量分析并采用数学模型来估计肾小球超滤系数（Kf）。来自健康女性肾移植供体的肾小球作为结构对照（N = 8）。
PET组的GFR低于对照水平，分别为91±23与149±34 ml/min/1.73 m²（P < 0.0001）。相比之下，两组的肾血浆流量和胶体渗透压相似（P =无显著性差异）。与对照组相比，PET组内皮窗孔密度和大小降低以及内皮下类纤维蛋白沉积物积聚降低了肾小球水力通透性，分别为1.81与2.58×10⁻⁹ m/sec/PA。系膜细胞插入也减少了有效滤过表面积。这些变化共同导致PET组计算得出的单个肾单位Kf低于对照组，分别为4.26与6.78 nl/min×mmHg。
单个肾单位Kf和GFR成比例（约40%）降低表明，PET中的滤过减少并非基于血流动力学，而是结构改变导致肾小球固有超滤能力受损的结果。
