Pathophysiology of preeclampsia: an angiogenic imbalance and long-lasting systemic vascular dysfunction

Preeclampsia is a systemic vascular disorder characterized by new-onset hypertension and proteinuria after 20 weeks of gestation. This condition targets several organs, including the kidneys, liver and brain, and is the leading cause of maternal and perinatal morbidity and mortality. Furthermore, re...

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Bibliographic Details
Published in:Hypertension research 2017-04, Vol.40 (4), p.305-310
Main Authors: Tomimatsu, Takuji, Mimura, Kazuya, Endo, Masayuki, Kumasawa, Keiichi, Kimura, Tadashi
Format: Article
Language:English
Subjects:
Cardiovascular disease
Endothelium, Vascular - physiopathology
Female
Humans
Hypertension
Kidney - physiopathology
Neovascularization, Pathologic - physiopathology
Pathogenesis
Pathophysiology
Pre-Eclampsia - etiology
Pre-Eclampsia - physiopathology
Preeclampsia
Pregnancy
Pregnancy complications
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Summary:Preeclampsia is a systemic vascular disorder characterized by new-onset hypertension and proteinuria after 20 weeks of gestation. This condition targets several organs, including the kidneys, liver and brain, and is the leading cause of maternal and perinatal morbidity and mortality. Furthermore, recent evidence has revealed preeclampsia as a significant risk factor for future cardiovascular diseases in these women. Over the past decade, increasing evidence has indicated that maternal angiogenic imbalances caused by placental antiangiogenic factors play a central role in the systemic vascular dysfunction underling preeclampsia. The severity of the maternal antiangiogenic state correlates closely with maternal and perinatal outcomes. Assessing angiogenic imbalance and several vascular function tests have also emerged as a way of detecting systemic vascular dysfunction during pregnancy. This review summarizes the current understanding of the pathophysiology of preeclampsia, its clinical applications and clinical evidence for future cardiovascular risks.
ISSN:0916-9636
1348-4214
DOI:10.1038/hr.2016.152