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子痫前期的发病机制。

Pathogenesis of preeclampsia.

作者信息

Sircar Monica, Thadhani Ravi, Karumanchi S Ananth

机构信息

aMassachusetts General Hospital and Harvard Medical School bBeth Israel Deaconess Medical Center and Harvard Medical School, Boston, Massachusetts, USA.

出版信息

Curr Opin Nephrol Hypertens. 2015 Mar;24(2):131-8. doi: 10.1097/MNH.0000000000000105.

DOI:10.1097/MNH.0000000000000105
PMID:25636145
Abstract

PURPOSE OF REVIEW

Preeclampsia is a gestational kidney disease characterized by glomerular endothelial injury, leading to maternal hypertension and proteinuria. If not addressed promptly, there is significant maternal and fetal morbidity and mortality. When severe, this disorder can cause hepatic and neurologic dysfunction. Understandably, this placental disease enters the focus of the obstetrician first; however, with progression, the nephrologist can also be enlisted. Typical complications include acute kidney injury, refractory hypertension, and acute pulmonary edema. This review summarizes recent literature on the pathogenesis of this condition and will highlight new diagnostic and therapeutic options for preeclampsia.

RECENT FINDINGS

Over the past decade, the role of soluble vascular factors in preeclampsia has shed light on the mechanism underlying this disease. During the last 2 years, several new therapeutics have been developed that target implicated circulating angiogenic factors, including soluble fms-like tyrosine kinase 1, an endogenous vascular endothelial growth factor inhibitor. Serum levels of angiogenic factors have been correlated with a constellation of hemodynamic and pathophysiologic changes. Thus, circulating levels of these factors may serve both diagnostic and prognostic purposes.

SUMMARY

Overall, our understanding of preeclampsia has developed significantly and the future holds promise for mechanism-based novel diagnostics and therapeutics.

摘要

综述目的

子痫前期是一种妊娠期肾脏疾病,其特征为肾小球内皮损伤,导致母体高血压和蛋白尿。若不及时处理,会出现严重的母婴发病和死亡情况。病情严重时,这种疾病可导致肝脏和神经功能障碍。可以理解的是,这种胎盘疾病首先会引起产科医生的关注;然而,随着病情进展,肾科医生也会参与进来。典型并发症包括急性肾损伤、难治性高血压和急性肺水肿。本综述总结了关于该病发病机制的近期文献,并将重点介绍子痫前期的新诊断和治疗方法。

最新发现

在过去十年中,可溶性血管因子在子痫前期中的作用揭示了该病的潜在机制。在过去两年里,已经开发出几种针对相关循环血管生成因子的新疗法,包括可溶性fms样酪氨酸激酶1,一种内源性血管内皮生长因子抑制剂。血管生成因子的血清水平与一系列血流动力学和病理生理变化相关。因此,这些因子的循环水平可能具有诊断和预后价值。

总结

总体而言,我们对子痫前期的认识有了显著进展,未来基于机制的新型诊断和治疗方法充满希望。

相似文献

1
Pathogenesis of preeclampsia.子痫前期的发病机制。
Curr Opin Nephrol Hypertens. 2015 Mar;24(2):131-8. doi: 10.1097/MNH.0000000000000105.
2
Excess placental soluble fms-like tyrosine kinase 1 (sFlt1) may contribute to endothelial dysfunction, hypertension, and proteinuria in preeclampsia.过量的胎盘可溶性fms样酪氨酸激酶1(sFlt1)可能导致子痫前期的内皮功能障碍、高血压和蛋白尿。
J Clin Invest. 2003 Mar;111(5):649-58. doi: 10.1172/JCI17189.
3
Circulating angiogenic factors in the pathogenesis and prediction of preeclampsia.循环血管生成因子在子痫前期发病机制及预测中的作用
Hypertension. 2005 Nov;46(5):1077-85. doi: 10.1161/01.HYP.0000187899.34379.b0. Epub 2005 Oct 17.
4
Pre-eclampsia: clinical manifestations and molecular mechanisms.子痫前期:临床表现与分子机制
Nephron Clin Pract. 2007;106(2):c72-81. doi: 10.1159/000101801. Epub 2007 Jun 6.
5
Soluble Fms-like tyrosine kinase 1 and endothelial dysfunction in the pathogenesis of preeclampsia.可溶性Fms样酪氨酸激酶1与子痫前期发病机制中的内皮功能障碍。
Pediatr Res. 2005 May;57(5 Pt 2):1R-7R. doi: 10.1203/01.PDR.0000159567.85157.B7. Epub 2005 Apr 6.
6
Preeclampsia: the role of angiogenic factors in its pathogenesis.子痫前期:血管生成因子在其发病机制中的作用
Physiology (Bethesda). 2009 Jun;24:147-58. doi: 10.1152/physiol.00043.2008.
7
Abnormal placentation, angiogenic factors, and the pathogenesis of preeclampsia.异常胎盘形成、血管生成因子与子痫前期发病机制。
Obstet Gynecol Clin North Am. 2010 Jun;37(2):239-53. doi: 10.1016/j.ogc.2010.02.013.
8
Angiogenic factors in the pathogenesis of preeclampsia.子痫前期发病机制中的血管生成因子。
Curr Top Dev Biol. 2005;71:297-312. doi: 10.1016/S0070-2153(05)71009-7.
9
Preeclampsia: an update.子痫前期:最新进展
Acta Anaesthesiol Belg. 2014;65(4):137-49.
10
Angiogenic factors and preeclampsia.血管生成因子与子痫前期
Thromb Res. 2009;123 Suppl 2:S93-9. doi: 10.1016/S0049-3848(09)70020-9.

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