期刊
JOURNAL OF DEVELOPMENTAL ORIGINS OF HEALTH AND DISEASE
卷 4, 期 5, 页码 411-420出版社
CAMBRIDGE UNIV PRESS
DOI: 10.1017/S2040174413000329
关键词
IUGR; renal development; uterine space restriction
资金
- NHLBI NIH HHS [R01 HL117341, R01 HL087144, R01 HL049210] Funding Source: Medline
- NICHD NIH HHS [P01 HD038843] Funding Source: Medline
Intrauterine growth restriction (IUGR) from uteroplacental dysfunction causes impaired nephrogenesis and ultimately hypertension, but it is unknown whether IUGR caused by insufficient space for placental development seen in uterine anomalies and/or multifetal gestation exerts the same effects. Fetal renal development and metabolism were studied in an ovine space-restriction model by combining unilateral horn surgical ligation and/or multifetal gestation. Reduced placental attachment sites and placental weight per fetus defined space-restricted (USR) v. control nonrestricted (NSR) fetuses. Space-restricted fetuses exhibited evidence for decreased plasma volume, with higher hematocrit and plasma albumin at gestational day (GD) 120, followed by lower blood pO(2), and higher osmolarity and creatinine at GD130, P<0.05 for all. By combining treatments, fetal kidney weight relative to fetal weight was inversely related to both fetal weight and plasma creatinine levels, P<0.05 for both. At GD130, space-restricted fetal kidney weights, cortical depths and glomerular generations were decreased, P<0.05 for all. Space-restricted kidneys underwent an adaptive response by prolonging active nephrogenesis and increasing maculae densa number, P<0.05 for both. The major renal adaptations in space-restricted IUGR fetuses included immaturity in both development and endocrine function, with evidence for impaired renal excretory function.
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