Developmental Origins of Chronic Renal Disease: An Integrative Hypothesis
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 recognize...
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| Format: | Article |
| Language: | English |
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Wiley
2013-01-01
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| Series: | International Journal of Nephrology |
| Online Access: | http://dx.doi.org/10.1155/2013/346067 |
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| author | F. Boubred M. Saint-Faust C. Buffat I. Ligi I. Grandvuillemin U. Simeoni |
| author_facet | F. Boubred M. Saint-Faust C. Buffat I. Ligi I. Grandvuillemin U. Simeoni |
| author_sort | F. Boubred |
| collection | DOAJ |
| description | 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. |
| format | Article |
| id | doaj-art-42b1bb075dd146658b88434ba5c2fd59 |
| institution | Kabale University |
| issn | 2090-214X 2090-2158 |
| language | English |
| publishDate | 2013-01-01 |
| publisher | Wiley |
| record_format | Article |
| series | International Journal of Nephrology |
| spelling | doaj-art-42b1bb075dd146658b88434ba5c2fd592025-02-03T01:31:02ZengWileyInternational Journal of Nephrology2090-214X2090-21582013-01-01201310.1155/2013/346067346067Developmental Origins of Chronic Renal Disease: An Integrative HypothesisF. Boubred0M. Saint-Faust1C. Buffat2I. Ligi3I. Grandvuillemin4U. Simeoni5Department of Neonatology, Assistance Publique-Hôpitaux de Marseille, Marseille, FranceDepartment of Neonatology, Assistance Publique-Hôpitaux de Marseille, Marseille, FranceAix-Marseille Université, Marseille, FranceDepartment of Neonatology, Assistance Publique-Hôpitaux de Marseille, Marseille, FranceDepartment of Neonatology, Assistance Publique-Hôpitaux de Marseille, Marseille, FranceDepartment of Neonatology, Assistance Publique-Hôpitaux de Marseille, Marseille, FranceCardiovascular 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.http://dx.doi.org/10.1155/2013/346067 |
| spellingShingle | F. Boubred M. Saint-Faust C. Buffat I. Ligi I. Grandvuillemin U. Simeoni Developmental Origins of Chronic Renal Disease: An Integrative Hypothesis International Journal of Nephrology |
| title | Developmental Origins of Chronic Renal Disease: An Integrative Hypothesis |
| title_full | Developmental Origins of Chronic Renal Disease: An Integrative Hypothesis |
| title_fullStr | Developmental Origins of Chronic Renal Disease: An Integrative Hypothesis |
| title_full_unstemmed | Developmental Origins of Chronic Renal Disease: An Integrative Hypothesis |
| title_short | Developmental Origins of Chronic Renal Disease: An Integrative Hypothesis |
| title_sort | developmental origins of chronic renal disease an integrative hypothesis |
| url | http://dx.doi.org/10.1155/2013/346067 |
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