Hostetter T H, Rosenberg M E
University of Minnesota, Minneapolis.
Am J Nephrol. 1990;10 Suppl 1:24-7. doi: 10.1159/000168190.
Glomerular capillary hemodynamics influence glomerular permselectivity to macromolecules, and alterations in these factors can evoke proteinuria. Changes in hemodynamic patterns can alter protein flux by changing its diffusion- or concentration-driven movement in the presence of a constant membrane barrier. Alternatively, hemodynamic forces may disrupt, transiently or irreversibly, the permeability characteristics of the capillary barrier. Maneuvers that lower glomerular capillary pressure appear capable of reversing at least in part, these latter permeability defects. Angiotensin II, provoked by higher levels of dietary protein intake, may be a particularly important mediator of proteinuria both through its effects on diffusion-mediated protein leakage and its tendency to provoke permeability defects due to heightening of glomerular capillary hydraulic pressures.
肾小球毛细血管血流动力学影响肾小球对大分子物质的滤过选择性，这些因素的改变可引发蛋白尿。血流动力学模式的变化可通过在恒定膜屏障存在的情况下改变其扩散或浓度驱动的运动来改变蛋白质通量。或者，血流动力学力可能会暂时或不可逆地破坏毛细血管屏障的通透性特征。降低肾小球毛细血管压力的措施似乎至少部分能够逆转这些通透性缺陷。由较高水平的膳食蛋白质摄入引发的血管紧张素II可能是蛋白尿的一个特别重要的介质，这是因为它对扩散介导的蛋白质渗漏有影响，并且由于肾小球毛细血管液压升高而有引发通透性缺陷的倾向。
