The implications of fetal programming of glomerular number and renal function

被引:33
作者
Doetsch, Joerg [1 ]
Plank, Christian [1 ]
Amann, Kerstin [2 ]
Ingelfinger, Julie [3 ]
机构
[1] Univ Erlangen Nurnberg, Dept Pediat Nephrol, D-91054 Erlangen, Germany
[2] Univ Erlangen Nurnberg, Dept Nephropathol, Erlangen, Germany
[3] Harvard Univ, Sch Med, Boston, MA USA
来源
JOURNAL OF MOLECULAR MEDICINE-JMM | 2009年 / 87卷 / 09期
关键词
Fetal; Epigenetics; Pediatrics; LOW-BIRTH-WEIGHT; INTRAUTERINE GROWTH-RETARDATION; CHANGE NEPHROTIC SYNDROME; RENIN-ANGIOTENSIN SYSTEM; FOR-GESTATIONAL-AGE; MATERNAL PROTEIN RESTRICTION; SOUTHEASTERN UNITED-STATES; NEWBORN KIDNEY SIZE; BLOOD-PRESSURE; 11-BETA-HYDROXYSTEROID DEHYDROGENASE;
D O I
10.1007/s00109-009-0507-7
中图分类号
Q3 [遗传学];
学科分类号
071007 ; 090102 ;
摘要
Large epidemiological studies suggest a clear relation between low birth weight and adverse renal outcomes evident as early as during childhood. Such adverse outcomes may include glomerular disease, hypertension, and renal failure. Data from autopsy material and from experimental models suggest that reduction in nephron number via diminished nephrogenesis may be a major mechanism, and factors that lead to this reduction are incompletely elucidated. Other mechanisms appear to be renal (e.g., via the intrarenal renin-angiotensin-aldosterone system) and nonrenal (e.g. changes in endothelial function). It also appears likely that the outcomes of fetal programming may be influenced postnatally, for example, by the amount of nutrients given at critical times.
引用
收藏
页码:841 / 848
页数:8
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