• J Natl Med Assoc · Nov 1998

    Rapid progression to end-stage renal disease in young hypertensive African Americans with proteinuria.

    • C I Obialo and K Hewan-Lowe.
    • Department of Medicine, Morehouse School of Medicine, Atlanta, Georgia 30310, USA.
    • J Natl Med Assoc. 1998 Nov 1; 90 (11): 649655649-55.

    AbstractHypertensive nephrosclerosis (HN) remains the most common cause of end-stage renal disease (ESRD) in blacks. This study examined whether renal histology corresponds with clinical hypertension in proteinuric blacks. Nondiabetic hypertensive blacks who satisfied inclusion criteria were enrolled in this study. Four male patients, each with a family history of hypertension and mean age 41 years, consented to kidney biopsy. Their mean arterial pressure was 116.5 mm Hg, mean urine protein excretion was 7.7 +/- 3.5 g/day. All patients progressed to ESRD within a mean duration of 14 months; the mean rate of decline in glomerular filtration rate was 53 mL/min/y, with an ESRD incidence of 80%/y. The histologic findings were consistent with previously described features of HN. Prominent glomerulosclerosis involved 30% to 75% of the glomeruli and extensive arteriolosclerosis/arteriosclerosis, tubular atrophy, and interstitial fibrosis. There was no evidence of immune complex disease by either immunofluorescence, electron microscopy, or serologic studies. The mean arterial pressure showed a strong but nonsignificant correlation with progression to ESRD (r = 0.8) and arteriosclerosis/arteriolosclerosis (r = 0.8). Glomerular sclerosis correlated with the reciprocal of serum creatinine (r = 0.6), interstitial fibrosis (r = 0.8), and arteriosclerosis/arteriolosclerosis (r = 0.3). Urine protein excretion correlated weakly with progression to ESRD (r = 0.4). These results indicate a poor correlation between clinical findings and histologic features on renal biopsy in young hypertensive African Americans. Hypertension remains a major cause of ESRD among African Americans, and progression to ESRD may be rapid in patients with marked proteinuria. Early and aggressive intervention is warranted.

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