We have found some years after apparent recovery from acute poststreptococcal glomerulonephritis (PSGN), features of continuing diseases are demonstrable as manifested by glomerular sclerosis, reductions in filtration rate, and exaggerated natriuresis in response to saline leading. The major objective of our study is to achieve a better understanding of the mechanism responsible for hypertension as it occurs in the course of chronic renal disease by a prospective study of these patients following PSGN, many of whom can be expected to become hypertensive. Our approach will consist of serial studies comparing normotensive and hypertensive patients following PSGN in regard to reduction in filtering bed, the nature and extent of glomerular and vascular changes histologically, their renal and systemic responses to acute and chronic salt loading, and to vasoconstrictor and vasodilator materials. A secondary objective is to evaluate the contribution of cellular immunity in the pathogenesis of chronicity in PSGN and other glomerular diseases, by examining lymphocytes for evidence of cellular hypersensitivity directed toward antigenic components of renal parenchyma, streptococcal antigens, glomerular basement membrane, mitogens and standard antigens.