INTRAUTERINE GROWTH-RETARDATION LEADS TO A PERMANENT NEPHRON DEFICIT IN THE RAT

被引：274

作者：

MERLETBENICHOU, C

GILBERT, T

MUFFATJOLY, M

LELIEVREPEGORIER, M

LEROY, B

机构：

[1] Unite de Recherches sur le Developpement Normal et Pathologique des Fonctions Epitheliales, INSERM U. 319, Université Paris 7, Paris, F-75251

来源：

PEDIATRIC NEPHROLOGY | 1994年 / 8卷 / 02期

关键词：

INTRAUTERINE GROWTH RETARDATION; NUMBER OF NEPHRONS; RENAL FUNCTION; COMPENSATORY HYPERTROPHY;

D O I：

10.1007/BF00865473

中图分类号：

R72 [儿科学];

学科分类号：

100202 ;

摘要：

Intrauterine growth retardation (IUGR) was induced in Sprague-Dawley rats by partial artery ligation of one uterine horn in the mother on day 17 of gestation or by feeding the mother a 5% protein diet from day 8 of gestation. The controls were pups of the contralateral uterine horn or pups born to mothers fed a normal (22%) protein diet. The number of nephrons present at birth and the final number of nephrons in 2-week-old rats were counted throughout the entire kidney. The number of nephrons present at birth and the final number of nephrons were significantly correlated with birth weight for growth-retarded rats of both groups and their corresponding controls (P <0.02 for the poorest correlation). Clearance experiments and morphometric studies of 2-week-old rats born to mothers with uterine artery ligation indicated that, despite a large compensatory hypertrophy of the nephrons in those animals born with a nephron deficit of about 30%, the overall renal function was impaired. We conclude that IUGR is accompanied by a nephron deficit which may not be fully compensated for within the first weeks after birth.

引用

页码：175 / 180

页数：6

共 36 条

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