Fetal origins of adult hypertension

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. Persistence of systemic and glomerular hypertension in adult life results in progressive glomerular sclerosis, further reducing FSA and thereby perpetuating a vicious cycle, leading, in the extreme, to end-stage renal failure. 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).