Hypertension has been presumed to cause end-organ damage in the kidney, and hypertension undoubtedly accelerates progressive scarring of renal parenchyma, but the relationship of hypertension and arterionephrosclero-sis is not simple and linear (11). In a large series of renal biopsies in patients with essential hypertension, arterionephrosclerosis was present in the vast majority, and the severity of arteriolar sclerosis correlated significantly with level of diastolic blood pressure (9). However, in several large autopsy series of patients with presumed benign hypertension, significant renal lesions were rare (4,5). Further, the level of blood pressure does not directly predict degree of end-organ damage: African-Americans have higher risk for more severe end-organ damage at any level of blood pressure (2). The African American Study of Kidney Disease (AASK) trial showed that African Americans with presumed arterionephrosclerosis indeed did not have other lesions, by renal biopsy, but the global sclerosis was severe and did not correlate with vascular sclerosis (12). It is possible that underlying microvascular disease causes the hypertension and the renal disease in susceptible patients. Underlying causes include possible genetic and structural components, such as decreased nephron number and consequently fewer, but enlarged glomeruli (13). Our data suggest a different phenotype of scarring in hypertensive nephrosclerosis in African Americans vs. Caucasians, with solidified global glomerulosclerosis prevalent in the former, contrasting with the obsolescent type (see above) in Caucasians (14). The AASK trial has shown that angiotensin-converting enzyme inhibitors (ACEIs) are effective in protecting renal function in African Americans, although multiple additional drugs were needed to achieve blood pressure control (15).
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