A large body of epidemiologic literature supports an inverse relation between birth weight and both systolic blood pressure and prevalence of hypertension, but mechanisms through which lower birth weight increases risk for hypertension are not established. This article advances the view that 1) permanently reduced nephron number is essential but not alone sufficient to mediate nutritionally induced hypertension; and 2) fetally programmed propensity for increased appetite and accelerated postnatal growth, thus generating inappropriately increased bodymass, is a necessary "second hit" to actualize hypertension vulnerability. Based on decades of nephrologic research, this increased ratio of bodymass (excretory load) to nephron number (excretory capacity) inducesintrarenalcompensations (tubular andglomerular hypertrophy with single-nephronhyperfiltration and intrarenal renin-angiotensin II activation), which maintain normal glomerular filtration rate at the expense of systemic and glomerular hypertension and at the risk of progressive renal disease. The vigor of the intrarenal compensatory responses is markedly greater in the immature than in the mature kidney, potentially explaining the greater risk of nephron deficits being present early in life as compared with the minimal risk in adult kidney donors. Effective interventions have not yet been defined. Suboptimalmaternal nutrition, pervasive in both developed and developing countries, offers a windowof opportunity to enhance the cardiovascular and renal health of future generations.
|Original language||English (US)|
|Number of pages||7|
|Journal||Journal of Nutrition|
|State||Published - Apr 1 2007|
ASJC Scopus subject areas
- Medicine (miscellaneous)
- Nutrition and Dietetics