The etiology of adult hypertension and progressive renal injury: an hypothesis

Abstract

We hypothesize 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 upon 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 epidemiological studies are needed to assess these initial impressions.