Early life obesity and chronic kidney disease in later life
The prevalence of chronic kidney disease (CKD) has increased considerably with a parallel rise in the prevalence of obesity. It is now recognized that early life nutrition has life-long effects on the susceptibility of an individual to develop obesity, diabetes, cardiovascular disease and CKD. The k...
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Veröffentlicht in: | Pediatric nephrology (Berlin, West) West), 2015-08, Vol.30 (8), p.1255-1263 |
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description | The prevalence of chronic kidney disease (CKD) has increased considerably with a parallel rise in the prevalence of obesity. It is now recognized that early life nutrition has life-long effects on the susceptibility of an individual to develop obesity, diabetes, cardiovascular disease and CKD. The kidney can be programmed by a number of intrauterine and neonatal insults. Low birth weight (LBW) is one of the most identifiable markers of a suboptimal prenatal environment, and the important intrarenal factors sensitive to programming events include decreased nephron number and altered control of the renin–angiotensin system (RAS). LBW complicated by accelerated catch-up growth is associated with an increased risk of obesity, hypertension and CKD in later life. High birth weight and exposure to maternal diabetes or obesity can enhance the risk for developing CKD in later life. Rapid postnatal growth per se may also contribute to the subsequent development of obesity and CKD regardless of birth weight and prenatal nutrition. Although the mechanisms of renal risks due to early life nutritional programming remain largely unknown, experimental and clinical studies suggest the burdening role of early life obesity in longstanding cardiovascular and renal diseases. |
doi_str_mv | 10.1007/s00467-014-2922-4 |
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It is now recognized that early life nutrition has life-long effects on the susceptibility of an individual to develop obesity, diabetes, cardiovascular disease and CKD. The kidney can be programmed by a number of intrauterine and neonatal insults. Low birth weight (LBW) is one of the most identifiable markers of a suboptimal prenatal environment, and the important intrarenal factors sensitive to programming events include decreased nephron number and altered control of the renin–angiotensin system (RAS). LBW complicated by accelerated catch-up growth is associated with an increased risk of obesity, hypertension and CKD in later life. High birth weight and exposure to maternal diabetes or obesity can enhance the risk for developing CKD in later life. Rapid postnatal growth per se may also contribute to the subsequent development of obesity and CKD regardless of birth weight and prenatal nutrition. 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It is now recognized that early life nutrition has life-long effects on the susceptibility of an individual to develop obesity, diabetes, cardiovascular disease and CKD. The kidney can be programmed by a number of intrauterine and neonatal insults. Low birth weight (LBW) is one of the most identifiable markers of a suboptimal prenatal environment, and the important intrarenal factors sensitive to programming events include decreased nephron number and altered control of the renin–angiotensin system (RAS). LBW complicated by accelerated catch-up growth is associated with an increased risk of obesity, hypertension and CKD in later life. High birth weight and exposure to maternal diabetes or obesity can enhance the risk for developing CKD in later life. Rapid postnatal growth per se may also contribute to the subsequent development of obesity and CKD regardless of birth weight and prenatal nutrition. Although the mechanisms of renal risks due to early life nutritional programming remain largely unknown, experimental and clinical studies suggest the burdening role of early life obesity in longstanding cardiovascular and renal diseases.</description><subject>Cardiovascular disease</subject><subject>Care and treatment</subject><subject>Chronic kidney failure</subject><subject>Complications and side effects</subject><subject>Development and progression</subject><subject>Educational Review</subject><subject>Humans</subject><subject>Kinases</subject><subject>Medicine</subject><subject>Medicine & Public Health</subject><subject>Nephrology</subject><subject>Nutrition</subject><subject>Obesity</subject><subject>Patient outcomes</subject><subject>Pediatric Obesity - complications</subject><subject>Pediatrics</subject><subject>Renal Insufficiency, Chronic - epidemiology</subject><subject>Renal Insufficiency, Chronic - etiology</subject><subject>Risk factors</subject><subject>Urology</subject><issn>0931-041X</issn><issn>1432-198X</issn><fulltext>true</fulltext><rsrctype>article</rsrctype><creationdate>2015</creationdate><recordtype>article</recordtype><sourceid>EIF</sourceid><sourceid>BENPR</sourceid><recordid>eNqF0kFrFDEYBuAgit1Wf4AXGRDEy9QvmcwkwVMptRYKXir0FjIzX3ZTs0lNZg777812W23LiuQQSJ73g4SXkHcUjimA-JwBeCdqoLxmirGavyALyhtWUyWvX5IFqIbWwOn1ATnM-QYAZCu71-SAtZS3TMCCfDkzyW8q7yxWscfspk1lwlgNqxSDG6qfbgy4qUaX0WSsXKi8mTDdBd6QV9b4jG_v9yPy4-vZ1em3-vL7-cXpyWU9CAZTjXyUKGGkTAwt9qo3trdcStFIEKgELUxKC1RaBX0ngALtgWMzdIq3Fpsj8mk39zbFXzPmSa9dHtB7EzDOWVOpyizVse7_tFO0Vaptm0I_PKM3cU6hPORONaor21-1NB61CzZOyQzbofqEN7IVChQUVe9RSwyYjI8BrSvHT_zxHl_WiGs37A18fBRYofHTKkc_Ty6G_BTSHRxSzDmh1bfJrU3aaAp6Wxq9K40updHb0mheMu_vf2Lu1zj-STy0pAC2A7lchSWmR1_1z6m_ARrqxrU</recordid><startdate>20150801</startdate><enddate>20150801</enddate><creator>Yim, Hyung Eun</creator><creator>Yoo, Kee Hwan</creator><general>Springer Berlin Heidelberg</general><general>Springer</general><general>Springer Nature B.V</general><scope>CGR</scope><scope>CUY</scope><scope>CVF</scope><scope>ECM</scope><scope>EIF</scope><scope>NPM</scope><scope>AAYXX</scope><scope>CITATION</scope><scope>3V.</scope><scope>7QP</scope><scope>7RV</scope><scope>7X7</scope><scope>7XB</scope><scope>88E</scope><scope>8AO</scope><scope>8FI</scope><scope>8FJ</scope><scope>8FK</scope><scope>ABUWG</scope><scope>AFKRA</scope><scope>AZQEC</scope><scope>BENPR</scope><scope>CCPQU</scope><scope>FYUFA</scope><scope>GHDGH</scope><scope>K9-</scope><scope>K9.</scope><scope>KB0</scope><scope>M0R</scope><scope>M0S</scope><scope>M1P</scope><scope>NAPCQ</scope><scope>PQEST</scope><scope>PQQKQ</scope><scope>PQUKI</scope><scope>PRINS</scope><scope>7X8</scope><scope>7TS</scope></search><sort><creationdate>20150801</creationdate><title>Early life obesity and chronic kidney disease in later life</title><author>Yim, Hyung Eun ; 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It is now recognized that early life nutrition has life-long effects on the susceptibility of an individual to develop obesity, diabetes, cardiovascular disease and CKD. The kidney can be programmed by a number of intrauterine and neonatal insults. Low birth weight (LBW) is one of the most identifiable markers of a suboptimal prenatal environment, and the important intrarenal factors sensitive to programming events include decreased nephron number and altered control of the renin–angiotensin system (RAS). LBW complicated by accelerated catch-up growth is associated with an increased risk of obesity, hypertension and CKD in later life. High birth weight and exposure to maternal diabetes or obesity can enhance the risk for developing CKD in later life. Rapid postnatal growth per se may also contribute to the subsequent development of obesity and CKD regardless of birth weight and prenatal nutrition. 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subjects | Cardiovascular disease Care and treatment Chronic kidney failure Complications and side effects Development and progression Educational Review Humans Kinases Medicine Medicine & Public Health Nephrology Nutrition Obesity Patient outcomes Pediatric Obesity - complications Pediatrics Renal Insufficiency, Chronic - epidemiology Renal Insufficiency, Chronic - etiology Risk factors Urology |
title | Early life obesity and chronic kidney disease in later life |
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