African-Americans have, in comparison with Caucasians, excess hypertension
and end-stage renal disease, which has been presumed to be due to hypertens
ion. However, systematic renal biopsy assessment of lesions in this populat
ion 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, w
ith glomerular filtration rate (GFR) between 25 and 70 mL/min per 1.73m(2)
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 5
1.7 +/- 13.6 mL/min per 1.73 m(2). Of these 39 biopsies, 38 showed arterios
clerosis 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 fiv
e biopsies, and in one patient, biopsy and clinical findings were consisten
t with idiopathic focal segmental glomerulosclerosis. Additional lesions in
cluded mesangiopathic glomerulonephritis in one patient, basement membrane
thickening suggestive of diabetic nephropathy in one, and cholesterol embol
i in two cases. Arteriolar and arterial sclerosis were tightly linked, and
correlated with interstitial fibrosis and the reciprocal of serum creatinin
e. Global glomerulosclerosis was extensive, involving on average 43 +/- 26%
of glomeruli. The extent of this lesion did not correlate with degree of a
rteriolar or arterial thickening, but did correlate with systolic blood pre
ssure (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 bas
ed on strict clinical criteria in non-diabetic African-Americans with mild
to moderate renal insufficiency without marked proteinuria is strongly corr
elated with renal biopsy vascular lesions consistent with this clinical dia
gnosis. However, the mechanism(s) for this clinicopathologic constellation
remains undetermined. Current studies are focused on possible genetic contr
ibutions to the development of hypertension and renal lesions in this popul
ation.