Shea S M, Raskova J, Morrison A B
Am J Pathol. 1980 Aug;100(2):513-28.
Subtotal nephrectomy in the rat gives rise to progressive proteinuria, glomerular hypertrophy, and glomerulosclerosis. The proteinuria antedates significant ultrastructural lesions demonstrable by conventional techniques; its mechanism is obscure. In this article it is shown that proteinuria in this system is not accompanied by evident changes in the ultrastructural distribution of anionic sites in the glomerular basement membrane, as determined by organ perfusion with two cationic probe molecules. It is suggested that the proteinuria may reflect a change in the steric aspect of glomerular ultrafilration, in which the loss of renal mass imposes a significant rise in capillary pressure in a structure whose capillaries are peculiar in the high pressures they normally sustain and in their lack of mechanical support from the interstitium. It is suggested that a sustained rise in capillary pressure overcomes the rigidity of the glomerular basement membrane, so that its pore size increases and proteinuria results from basement membrane failure.
大鼠肾次全切除会导致进行性蛋白尿、肾小球肥大和肾小球硬化。蛋白尿早于传统技术可显示的明显超微结构病变出现;其机制尚不清楚。本文表明,通过用两种阳离子探针分子进行器官灌注测定,该系统中的蛋白尿并未伴有肾小球基底膜阴离子位点超微结构分布的明显变化。有人提出,蛋白尿可能反映了肾小球超滤空间方面的变化,其中肾实质的丧失使一种结构中的毛细血管压力显著升高,该结构的毛细血管具有正常承受高压且缺乏来自间质的机械支撑的特殊之处。有人提出,毛细血管压力的持续升高克服了肾小球基底膜的刚性,从而使其孔径增大,蛋白尿因基底膜功能障碍而产生。