Influence of arteriolar hyalinization on arterial intimal fibroplasia in the renal cortex of subjects in the United States, Peru, and Bolivia, applicable also to other populations.

Microvasculopathies of nephrosclerosis progress with age in contrasting patterns. Arterial intimal fibroplasia (R(r) and R(c), respectively, in small and large interlobular arteries) previously showed close linkages to hypertension and to "nephrosclerosis," defined by fibrous replacement of atrophied nephrons, whereas hyalinization of arterioles (Hy) failed to show consistent linkages. In this study, renal samples from seven populations, three newly assembled and four reassessed from archived data, were evaluated for R(r), R(c), and Hy in forensic autopsies of basal subjects (ie, those lacking conditions known to correlate with hypertension or nephrosclerosis, mostly deaths by violence). The patterns of progression on age were alike in all populations, but the rates of progression differed greatly. The observed ranges indicate a 547% higher rate for Hy in the fastest compared with the slowest population, a 49% higher rate for R(c), and a 107% higher rate for R(r). About one third of variation in R(r) and R(c) between populations can be attributed to the correlation with Hy, leaving a substantial residual effect independent of Hy. The findings suggest that the etiology propelling hyalinization in arterioles seems somehow to accelerate the progression of intimal fibroplasia in arteries. The reverse direction, fibroplasia somehow accelerating hyalinization, seems unreasonable, because the presumed consequence, Hy, fails to increase notably with age after 40 years, whereas the presumed causes, R(r) and R(c), rise unremittingly into old age. The etiologies of the population differences are of great consequence to public health but remain unknown.