Progression of Renal Disease

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To the Editor: Klahr et al. (June 23 issue)1 have done an admirable job of discussing the multiple abnormalities seen in progressive renal disease. I would like to add that several lines of evidence suggest that during hyperfiltration, intrarenal levels of angiotensin II may be increased,2 thereby explaining the apparent efficacy of converting-enzyme inhibition in several experimental models of kidney failure. First, the number of angiotensin II receptors is reduced in the glomerulus of diabetic rats3; such a reduction (i.e., down-regulation) generally occurs in the presence of increased concentrations of that hormone. Second, in nearly all forms of progressive . . .