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Developmental Origins of Chronic Renal Disease: An Integrative Hypothesis

DOI: 10.1155/2013/346067

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Abstract:

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. 1. Introduction Cardiovascular diseases ((CVD) hypertension, coronary disease and stroke, and heart failure) are one of the leading causes of mortality in industrialized countries, and the prevalence is increasing in emerging societies. All cardiovascular diseases account for 4.3 million deaths per year in the European Union, and the prevalence of chronic heart failure in the United States of America is approximately 6 million [1, 2]. In industrialized countries, hypertension (HT) affects 25% to 35% of the global population and reaches 60% to 70% of the population aged 60 or more. Hypertension is the principal risk factor of death worldwide [3]. It increases the severity of ischemic vascular diseases and, with obesity and type 2 diabetes, is one of the important risk factors for chronic kidney disease (CKD). Chronic kidney disease is defined as reduced glomerular filtration rate (GFR) up to end-stage renal disease (ESRD), proteinuria, or both. Prevalence of ESRD, estimated to be 0.5–2.5‰ worldwide, is increasing in several countries [4]. In turn, impaired renal factor favors the development of and amplifies the severity of CVD [5–7]. During the last two decades, it has been raised the concept of developmental programming of adult chronic

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