Abstract
Arterionephrosclerosis is diagnosed at autopsy by assessing the severity and extent of certain structural features in the renal cortical arteries seen in tissue sections. These features are characterized by fibrotic intimal thickening and medial shrinkage, a progressive change from the youthful muscular pattern to the elderly sclerotic pattern. Intimal fibrosis can be quantified by expressing intimal thickness as a percentage of the arterial outer diameter (% OD). The magnitude of arterionephrosclerosis, found by averaging the measures of intimal fibrosis seen in a kidney, can be calculated from age and mean blood pressure, using a standard prediction function. This function is a quantitative statement of a fundamentally important principle: just as blood pressure is a continuous variable that can range from low to high levels, arterionephrosclerosis is also a continuous variable that can take any degree of abnormality of arterial structure from minimal to maximal. Furthermore, a correspondence exists between the two quantities so that each can be calculated from the other. In this study, a correlation of 0.966 was found between the observed and the calculated magnitudes of arterionephrosclerosis over 10-year age groups from 25 to 34 years to 65 to 74 years, using group average data within age groups. For individuals, however, the correlations between observed and calculated magnitudes of arterionephrosclerosis were about 0.6 in a former study of elderly subjects and about 0.1 in the subjects aged 6 to 27 years in this study. The average growth rate of arterionephrosclerosis was found to be about 0.25 %OD per year from ages 15 to 54 years, and about 0.13 %OD per year from ages 55 to 70 years; the growth rate did not increase in the oldest age groups when blood pressure averaged higher than blood pressure in more youthful subjects. These and other findings are consistent with the view that the reason a correlation exists between blood pressure and arterionephrosclerosis could be because the magnitude of arterionephrosclerosis is one of the determinants that sets the level of blood pressure. From this perspective, each individual can be viewed as having other determinants of blood pressure, methodologic or biologic, which add to or subtract from the values set by age and arterionephrosclerosis. When subjects are pooled into groups, so that individual determinants balance out, the group average levels of mean blood pressure could be interpreted as reflecting little other than the magnitude of arterionephrosclerosis at each specific age.
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