Fetal programming of renal function

被引:21
|
作者
Doetsch, Joerg [1 ]
Plank, Christian [2 ]
Amann, Kerstin [3 ]
机构
[1] Univ Cologne, Dept Pediat, D-50937 Cologne, Germany
[2] Univ Erlangen Nurnberg, Dept Pediat, D-91054 Erlangen, Germany
[3] Univ Erlangen Nurnberg, Dept Nephropathol, D-91054 Erlangen, Germany
关键词
Fetal programming; Low birth weight; Glomerulonephritis; Chronic renal failure; Nephrotic syndrome; Diabetes mellitus; LOW-BIRTH-WEIGHT; INTRAUTERINE GROWTH-RETARDATION; MATERNAL PROTEIN RESTRICTION; CHANGE NEPHROTIC SYNDROME; RENIN-ANGIOTENSIN SYSTEM; FOR-GESTATIONAL-AGE; 11-BETA-HYDROXYSTEROID DEHYDROGENASE TYPE-2; SOUTHEASTERN UNITED-STATES; HENOCH-SCHONLEIN NEPHRITIS; ADULT-BLOOD PRESSURE;
D O I
10.1007/s00467-011-1781-5
中图分类号
R72 [儿科学];
学科分类号
100202 ;
摘要
Results from large epidemiological studies suggest a clear relation between low birth weight and adverse renal outcome evident as early as during childhood. Such adverse outcomes may include glomerular disease, hypertension, and renal failure and contribute to a phenomenon called fetal programming. Other factors potentially leading to an adverse renal outcome following fetal programming are maternal diabetes mellitus, smoking, salt overload, and use of glucocorticoids during pregnancy. However, clinical data on the latter are scarce. Here, we discuss potential underlying mechanisms of fetal programming, including reduced nephron number via diminished nephrogenesis and other renal (e.g., via the intrarenal renin-angiotensin-aldosterone system) and non-renal (e.g., changes in endothelial function) alterations. It appears likely that the outcomes of fetal programming may be influenced or modified postnatally, for example, by the amount of nutrients given at critical times.
引用
收藏
页码:513 / 520
页数:8
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