Fetal and perinatal programming of renal function

被引：0

作者：

Dötsch J. ^{[1
]}

机构：

[1] Klinik und Poliklinik für Kinder- und Jugendmedizin, Uniklinik Köln, 50937 Köln

来源：

Gynäkologische Endokrinologie | 2014年 / 12卷 / 2期

关键词：

Birth weight; Glomerular filtration rate; Intrauterine environment; Intrauterine growth retardation; Pregnancy;

D O I：

10.1007/s10304-013-0593-z

中图分类号：

学科分类号：

摘要：

Impact. Low birth weight is associated with reduced renal function which is sometimes already present in childhood. Among the diseases that are encountered more frequently or are more severe are glomerular diseases, hypertension, and chronic kidney disease. Causes. A potential cause of this phenomenon is fetal programming which is defined as a permanent alteration of biological function by a temporary intrauterine event. However, low birth weight is not the only factor influencing renal function via fetal programming. Other factors include maternal diabetes, maternal smoking, high salt intake, and the administration of glucocorticoids during pregnancy. Mechanisms. Possible mechanisms that may be involved are impaired nephrogenesis, which is represented by a diminished number of nephrons and other renal and extrarenal mechanisms. Human and animal data suggest that the consequences of fetal programming are influenced by the postnatal environment to a large extent. One of those postnatal modifiers appears to be nutrition in infancy and early childhood. © 2014 Springer-Verlag.

引用

页码：87 / 92

页数：5

共 72 条

[21]

Howles S.A., Edwards M.H., Cooper C., Thakker R.V., Kidney stones: A fetal origins hypothesis, J Bone Miner Res, 28, pp. 2535-2539, (2013)

[22]

Stoffers D.A., Desai B.M., DeLeon D.D., Simmons R.A., Neonatal exendin-4 prevents the development of diabetes in the intrauterine growth retarded rat, Diabetes, 52, 3, pp. 734-740, (2003)

[23]

Nusken K.-D., Dotsch J., Rauh M., Rascher W., Schneider H., Uteroplacental insufficiency after bilateral uterine artery ligation in the rat: Impact on postnatal glucose and lipid metabolism and evidence for metabolic programming of the offspring by sham operation, Endocrinology, 149, 3, pp. 1056-1063, (2008)

[24]

Woods L.L., Ingelfinger J.R., Nyengaard J.R., Rasch R., Maternal protein restriction suppresses the newborn renin-angiotensin system and programs adult hypertension in rats, Pediatric Research, 49, 4 I, pp. 460-467, (2001)

[25]

Elmes M.J., Gardner D.S., Langley-Evans S.C., Fetal exposure to a maternal low-protein diet is associated with altered left ventricular pressure response to ischaemia-reperfusion injury, British Journal of Nutrition, 98, 1, pp. 93-100, (2007)

[26]

Plank C., Ostreicher I., Hartner A., Marek I., Struwe F.G., Amann K., Hilgers K.F., Rascher W., Dotsch J., Intrauterine growth retardation aggravates the course of acute mesangioproliferative glomerulonephritis in the rat, Kidney International, 70, 11, pp. 1974-1982, (2006)

[27]

Wlodek M.E., Westcott K., Siebel A.L., Owens J.A., Moritz K.M., Growth restriction before or after birth reduces nephron number and increases blood pressure in male rats, Kidney International, 74, 2, pp. 187-195, (2008)

[28]

Plank C., Nusken K.D., Menendez-Castro C., Et al., Intrauterine growth restriction following ligation of the uterine arteries leads to more severe glomerulosclerosis after mesangioproliferative glomerulonephritis in the offspring, Am J Nephrol, 32, pp. 287-295, (2010)

[29]

Langley-Evans S.C., Nutritional programming of disease: Unravelling the mechanism, J Anat, 215, pp. 36-51, (2009)

[30]

Nuyt A.M., Mechanisms underlying developmental programming of elevated blood pressure and vascular dysfunction: Evidence from human studies and experimental animal models, Clin Sci (Lond), 114, pp. 1-17, (2008)

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