• 1 January 1980
    • journal article
    • research article
    • Vol. 100  (2) , 513-+
Abstract
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 sytem is not accompanied by evident changes in the ultrastructural distribution of anionic sites in the glomerular basement membrane, as determined by organ perfusion with 2 cationic probe molecules. The proteinuria may reflect a change in the steric aspect of glomerular ultrafiltration, 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. A sustained rise in capillary pressure may overcome the rigidity of the glomerular basement membrane, so that its pore size increases and proteinuria results from basement membrane failure.