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      Developmental Origins and Nephron Endowment in Hypertension

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          Abstract

          Primary hypertension continues to be one of the main risk factors for cardiovascular disease worldwide. A stable intrauterine environment is critical for the future development and health of the fetus. The developing kidney has been found to be especially vulnerable during this time period, and epidemiological studies have demonstrated that an adverse in utero environment is associated with an increased risk of hypertension and chronic kidney disease. Macro- and micronutrient deficiencies as well as exposure to tobacco, alcohol, and certain medications during gestation have been shown to negatively impact nephrogenesis and reduce one’s nephron number. In 1988, Brenner et al. put forth the controversial hypothesis that a reduced nephron complement is a risk factor for hypertension and chronic kidney disease in adulthood. Since then numerous animal and human studies have confirmed this relationship demonstrating that there is an inverse association between blood pressure and nephron number. As our understanding of the developmental programming of hypertension and other non-communicable diseases improves, more effective preventive health measures can be developed in the future.

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          Most cited references64

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          A comparative risk assessment of burden of disease and injury attributable to 67 risk factors and risk factor clusters in 21 regions, 1990–2010: a systematic analysis for the Global Burden of Disease Study 2010

          The Lancet, 380(9859), 2224-2260
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            Fetal origins of coronary heart disease.

            The fetal origins hypothesis states that fetal undernutrition in middle to late gestation, which leads to disproportionate fetal growth, programmes later coronary heart disease. Animal studies have shown that undernutrition before birth programmes persisting changes in a range of metabolic, physiological, and structural parameters. Studies in humans have shown that men and women whose birth weights were at the lower end of the normal range, who were thin or short at birth, or who were small in relation to placental size have increased rates of coronary heart disease. We are beginning to understand something of the mechanisms underlying these associations. The programming of blood pressure, insulin responses to glucose, cholesterol metabolism, blood coagulation, and hormonal settings are all areas of active research.
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              Global burden of hypertension: analysis of worldwide data

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                Author and article information

                Contributors
                Journal
                Front Pediatr
                Front Pediatr
                Front. Pediatr.
                Frontiers in Pediatrics
                Frontiers Media S.A.
                2296-2360
                29 June 2017
                2017
                : 5
                : 151
                Affiliations
                [1] 1Department of Pediatrics, Division of Pediatric Nephrology, Cohen Children’s Medical Center of New York , New York, NY, United States
                Author notes

                Edited by: Ibrahim F. Shatat, MUSC – WCMC – Sidra Medical and Research Center, Qatar

                Reviewed by: Kimberly Jean Reidy, Albert Einstein College of Medicine, United States; Kirtida Mistry, Children’s National Medical Center, United States

                *Correspondence: Christine B. Sethna, csethna@ 123456northwell.edu

                Specialty section: This article was submitted to Pediatric Nephrology, a section of the journal Frontiers in Pediatrics

                Article
                10.3389/fped.2017.00151
                5489607
                28706894
                42243968-235d-4c49-b483-634a028018d7
                Copyright © 2017 Gurusinghe, Tambay and Sethna.

                This is an open-access article distributed under the terms of the Creative Commons Attribution License (CC BY). The use, distribution or reproduction in other forums is permitted, provided the original author(s) or licensor are credited and that the original publication in this journal is cited, in accordance with accepted academic practice. No use, distribution or reproduction is permitted which does not comply with these terms.

                History
                : 29 March 2017
                : 15 June 2017
                Page count
                Figures: 2, Tables: 0, Equations: 0, References: 79, Pages: 8, Words: 6275
                Categories
                Pediatrics
                Review

                hypertension,nephron,fetal origins hypothesis,low birth weight,blood pressure

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