Abstract
Summary: African‐Americans have, in comparison with Caucasians, excess hypertension and end‐stage renal disease, which has been presumed to be due to hypertension. However, systematic renal biopsy assessment of lesions in this population and verification of this clinical impression have not been done. During the pilot phase of the AASK trial, 46 hypertensive (diastolic BP > 95 mmHg) non‐diabetic African‐American patients between the ages of 18–70 years, with glomerular filtration rate (GFR) between 25 and 70 mL/min per 1.73m2 and without marked proteinuria were therefore biopsied to assess underlying lesions. Adequate biopsy material was obtained in 39 (29 men and 10 women), on average 53.0 ± 11.0 years old, with MAP of 109 ± 15 mmHg and GFR 51.7 ± 13.6 mL/min per 1.73 m2. of these 39 biopsies, 38 showed arteriosclerosis and/or arteriolosclerosis, severity on average 1.5 ± 0.9 and 1.5 ± 0.8, respectively, on a 0–3+ scale. Interstitial fibrosis was moderate, 1.3 ± 0.9 (0–3+ scale). Segmental glomerulosclerosis was present in five biopsies, and in one patient, biopsy and clinical findings were consistent with idiopathic focal segmental glomerulosclerosis. Additional lesions included mesangiopathic glomerulonephritis in one patient, basement membrane thickening suggestive of diabetic nephropathy in one, and cholesterol emboli in two cases. Arteriolar and arterial sclerosis were tightly linked, and correlated with interstitial fibrosis and the reciprocal of serum creatinine. Global glomerulosclerosis was extensive, involving on average 43 ± 26% of glomeruli. the extent of this lesion did not correlate with degree of arteriolar or arterial thickening, but did correlate with systolic blood pressure (P 0.0174), the reciprocal of serum creatinine (P= 0.0009), serum cholesterol (P= 0.0129) and interstitial fibrosis (P < 0.0001). These data underscore that the clinical diagnosis of hypertensive nephrosclerosis based on strict clinical criteria in non‐diabetic African‐Americans with mild to moderate renal insufficiency without marked proteinuria is strongly correlated with renal biopsy vascular lesions consistent with this clinical diagnosis. However, the mechanism(s) for this clinicopathologic constellation remains undetermined. Current studies are focused on possible genetic contributions to the development of hypertension and renal lesions in this population.
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