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International Journal of Nephrology
Volume 2013, Article ID 346067, 12 pages
Review Article

Developmental Origins of Chronic Renal Disease: An Integrative Hypothesis

1Department of Neonatology, Assistance Publique-Hôpitaux de Marseille, Marseille, France
2Aix-Marseille Université, Marseille, France
3Aix-Marseille Université, UMR-S 1076 INSERM, Marseille, France

Received 27 March 2013; Revised 17 June 2013; Accepted 3 July 2013

Academic Editor: Anil K. Agarwal

Copyright © 2013 F. Boubred et al. This is an open access article distributed under the Creative Commons Attribution License, which permits unrestricted use, distribution, and reproduction in any medium, provided the original work is properly cited.


Cardiovascular diseases are one of the leading causes of mortality. Hypertension (HT) is one of the principal risk factors associated with death. Chronic kidney disease (CKD), which is probably underestimated, increases the risk and the severity of adverse cardiovascular events. It is now recognized that low birth weight is a risk factor for these diseases, and this relationship is amplified by a rapid catch-up growth or overfeeding during infancy or childhood. The pathophysiological and molecular mechanisms involved in the “early programming” of CKD are multiple and partially understood. It has been proposed that the developmental programming of arterial hypertension and chronic kidney disease is related to a reduced nephron endowment. However, this mechanism is still discussed. This review discusses the complex relationship between birth weight and nephron endowment and how early growth and nutrition influence long term HT and CKD. We hypothesize that fetal environment reduces moderately the nephron number which appears insufficient by itself to induce long term diseases. Reduced nephron number constitutes a “factor of vulnerability” when additional factors, in particular a rapid postnatal growth or overfeeding, promote the early onset of diseases through a complex combination of various pathophysiological pathways.