Adverse consequences of accelerated neonatal growth: cardiovascular and renal issues
Abstract Epidemiological and experimental studies show that the risk of cardiovascular and metabolic diseases at adulthood is inversely related to the weight at birth. Although with less evidence, low birth weight has been suggested to increase the risk of chronic kidney disease (CKD). It is well established that the developmental programming of arterial hypertension and of renal disease involves in particular renal factors, especially nephron endowment, which is reduced in low birth weight and maternal diabetes situations. Experimental studies, especially in rodents, have demonstrated the long-term influence of postnatal nutrition and/or postnatal growth on cardiovascular, metabolic and renal functions, while human data are scarce on this issue. Vascular and renal diseases appear to have a “multihits” origin, with reduced nephron number the initial hit and rapid postnatal growth the second hit. This review addresses the current understanding of the role of the kidney, both as a mechanism and as a target, in the developmental origins of adult disease theory, with a particular focus on the long-term effects of postnatal growth and nutrition..
| Medienart: |
E-Artikel |
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| Erscheinungsjahr: |
2010 |
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| Erschienen: |
2010 |
| Enthalten in: |
Zur Gesamtaufnahme - volume:26 |
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| Enthalten in: |
Pediatric nephrology - 26(2010), 4 vom: 12. Okt., Seite 493-508 |
| Sprache: |
Englisch |
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| Beteiligte Personen: |
Simeoni, Umberto [VerfasserIn] |
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| Links: |
Volltext [lizenzpflichtig] |
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| BKL: | |
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| Themen: |
Chronic kidney disease |
| RVK: |
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| Anmerkungen: |
© IPNA 2010 |
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| doi: |
10.1007/s00467-010-1648-1 |
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| funding: |
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| 245 | 1 | 0 | |a Adverse consequences of accelerated neonatal growth: cardiovascular and renal issues |
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| 520 | |a Abstract Epidemiological and experimental studies show that the risk of cardiovascular and metabolic diseases at adulthood is inversely related to the weight at birth. Although with less evidence, low birth weight has been suggested to increase the risk of chronic kidney disease (CKD). It is well established that the developmental programming of arterial hypertension and of renal disease involves in particular renal factors, especially nephron endowment, which is reduced in low birth weight and maternal diabetes situations. Experimental studies, especially in rodents, have demonstrated the long-term influence of postnatal nutrition and/or postnatal growth on cardiovascular, metabolic and renal functions, while human data are scarce on this issue. Vascular and renal diseases appear to have a “multihits” origin, with reduced nephron number the initial hit and rapid postnatal growth the second hit. This review addresses the current understanding of the role of the kidney, both as a mechanism and as a target, in the developmental origins of adult disease theory, with a particular focus on the long-term effects of postnatal growth and nutrition. | ||
| 650 | 4 | |a Low birth weight | |
| 650 | 4 | |a Nephron number | |
| 650 | 4 | |a Postnatal catch-up growth | |
| 650 | 4 | |a Vascular disease | |
| 650 | 4 | |a Chronic kidney disease | |
| 650 | 4 | |a Glomerular sclerosis | |
| 650 | 4 | |a Developmental programming | |
| 650 | 4 | |a Developmental origins of adult disease | |
| 700 | 1 | |a Ligi, Isabelle |4 aut | |
| 700 | 1 | |a Buffat, Christophe |4 aut | |
| 700 | 1 | |a Boubred, Farid |4 aut | |
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