Congenital Oligonephropathy and the Etiology of Adult Hypertension and Progressive Renal Injury
American Journal of Kidney DiseasesPublished 1 February 1994
Barry M. Brenner, Glenn M. Chertow
Citations599
SJR quartileQ1
SJR score3.02
SNIP2.94
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TL;DR
It is hypothesized that retardation of renal development as occurs in individuals of low birth weight gives rise to increased postnatal risks for systemic and glomerular hypertension as well as enhanced risk of expression of renal disease.
Abstract
Based on the associations reviewed in this report, we have hypothesized that retardation of renal development as occurs in individuals of low birth weight gives rise to increased postnatal risks for systemic and glomerular hypertension as well as enhanced risk of expression of renal disease. This hypothesis draws on observations suggesting (1) a direct relationship between birth weight and nephron number, (2) an inverse relationship between birth weight and later-life hypertension, and (3) an inverse relationship between nephron number and blood pressure, irrespective of whether nephron number is reduced congenitally or in postnatal life (as from partial renal ablation or acquired renal disease). Additional clinical and epidemiologic studies are needed to assess these initial impressions.
Keywords
MedicineBiochemistry, Genetics and Molecular Biology
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