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目的：探讨米非司酮对人胎肾组织超微结构的影响。方法：将中孕期引产的病例分为米非司酮组与对照组，每组各５例，胎龄为１８ ～２１ 孕周。米非司酮组在引产前６ ｈ 服用１５０ ｍｇ 米非司酮，然后行水囊引产术，对照组则只行水囊引产术。胎儿娩出后，取肾组织进行样品制备以供透射电镜观察。结果：与对照组相比，在米非司酮引产的胎肾组织可见下列形态改变：（１） 血管球的内皮肿胀，胞膜破裂，核浓缩及碎裂；（２） 肾小囊脏层足细胞水肿明显，部分胞膜破裂；（３） 肾近端小管上皮水肿，线粒体呈基质型肿胀；（４） 肾远端小管上皮胞浆膨出及破裂，线粒体常呈基质型肿胀，嵴型肿胀少见；（５） 集合小管的上皮细胞水肿，线粒体以嵴型肿胀为主；（６） 间质结构松弛，血管上皮缺损及成纤维细胞水肿。结论：米非司酮可造成胎肾组织缺氧性损伤。因此，米非司酮于晚期引产有可能给新生儿留下肾功能损伤的后遗症
Objective: To investigate the effect of mifepristone on the ultrastructure of human fetal kidney. Methods: The cases of induced labor in the second trimester were divided into the mifepristone group and the control group, with 5 cases in each group. The gestational age ranged from 18 to 21 gestational weeks. In the mifepristone group, 150 mg of mifepristone was administered 6 h before induction of labor, and then the water bag was used for induction of labor. In the control group, only water bag induction was performed. After the fetus was delivered, the kidney tissues were taken for sample preparation for transmission electron microscopy. RESULTS: Compared with the control group, the following morphological changes were observed in the fetal tissue of the fetus induced by mifepristone: (1) endothelial swelling of the glomerulus, rupture of the membrane, nuclear condensation and fragmentation; (2) Podocyte edema is obvious, some of the cell membrane rupture; (3) renal proximal tubule epithelial edema, mitochondrial matrix was swollen; (4) tubular distal tubular epithelial cytoplasm bulging and rupture, mitochondria often matrix-like swelling, ridge type Swelling is rare; (5) epithelial cell edema of collecting tubules, mitochondria dominated by ridge swelling; (6) interstitial structure relaxation, vascular epithelial defects and fibroblast edema. Conclusion: Mifepristone can cause hypoxia damage in fetal kidney tissue. Therefore, mifepristone in late induction of labor may leave neonatal sequelae of renal damage