Pre-eclampsia part 1: current understanding of its pathophysiology

Chaiworapongsa, Tinnakorn; Chaemsaithong, Piya; Yeo, Lami; Romero, Roberto

doi:10.1038/nrneph.2014.102

Cited by 956Pregnancy and preeclampsia studiesNeurological Complications and SyndromesReproductive System and Pregnancy

Pre-eclampsia part 1: current understanding of its pathophysiology

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Chaiworapongsa, Tinnakorn, Chaemsaithong, Piya, Yeo, Lami, Romero, Roberto·2014·Nature Reviews Nephrology

DOI 10.1038/nrneph.2014.102PMC PMC5893150

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Abstract

Pre-eclampsia is characterized by new-onset hypertension and proteinuria at ≥20 weeks of gestation. In the absence of proteinuria, hypertension together with evidence of systemic disease (such as thrombocytopenia or elevated levels of liver transaminases) is required for diagnosis. This multisystemic disorder targets several organs, including the kidneys, liver and brain, and is a leading cause of maternal and perinatal morbidity and mortality. Glomeruloendotheliosis is considered to be a characteristic lesion of pre-eclampsia, but can also occur in healthy pregnant women. The placenta has an essential role in development of this disorder. Pathogenetic mechanisms implicated in pre-eclampsia include defective deep placentation, oxidative and endoplasmic reticulum stress, autoantibodies to type-1 angiotensin II receptor, platelet and thrombin activation, intravascular inflammation, endothelial dysfunction and the presence of an antiangiogenic state, among which an imbalance of angiogenesis has emerged as one of the most important factors. However, this imbalance is not specific to pre-eclampsia, as it also occurs in intrauterine growth restriction, fetal death, spontaneous preterm labour and maternal floor infarction (massive perivillous fibrin deposition). The severity and timing of the angiogenic imbalance, together with maternal susceptibility, might determine the clinical presentation of pre-eclampsia. This Review discusses the diagnosis, classification, clinical manifestations and putative pathogenetic mechanisms of pre-eclampsia.

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The increase of sVEGFR-1 causes a parallel decrease of maternal plasma concentrations of PlGF in preeclampsia.
“The increase of sVEGFR-1 causes a parallel decrease of maternal plasma concentrations of PIGF in preeclampsia(119, 143–150).”
From Metformin, the Aspirin of the 21st Century: Its Role in Gestational Diabetes Mellitus, Prevention of Preeclampsia and Cancer, and the Promotion of Longevity (2017) · cites this paper as [143]

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[20]Kenny LC Baker PN Cunningham FG Chesley’s Hypertensive Disorders in Pregnancy Lindheimer MD Roberts JM Cunningham GC 335 351 Elsevier 2009
[21]Lindheimer MD Roberts JM Cunningham GC Chesley L Chesley’s Hypertensive Disorders in Pregnancy Lindheimer MD Roberts JM Cunningham GC 25 36 Elsevier 2009
[33]Ward K Lindheimer MD Chesley’s Hypertensive Disorders in Pregnancy Lindheimer MD Roberts JM Cunningham GC 51 71 Elsevier 2009
[69]Brosens IA Robertson WB Dixon HG The role of the spiral arteries in the pathogenesis of preeclampsia Obstet. Gynecol. Annu 1 177 191 1972 4669123
[110]Dechend R Luft FC Lindheimer M Chesley’s Hypertensive Disorders in Pregnancy Lindheimer MD Roberts JM Cunningham GC 287 296 Elsevier 2009
[192]Leveno KJ Cunningham FG Chesley’s Hypertensive Disorders in Pregnancy Lindheimer MD Roberts JM Cunningham GC 389 414 Elsevier 2009

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Authors: Chaiworapongsa, T., Chaemsaithong, P., Yeo, L., & Romero, R.
Affiliations: National Institutes of Health (US)
Corresponding author: Chaiworapongsa, Tinnakorn
ORCID: Chaiworapongsa, Tinnakorn
Chaemsaithong, Piya
Yeo, Lami
Romero, Roberto
Venue: Nature Reviews Nephrology
Publisher: Springer Science and Business Media LLC
Published: 2014-07-08
Volume: 10
Issue: 8
Pages: 466-480
ISSN: 1745-8323 (ISSN-L)
1759-5061
1759-507X
DOI: 10.1038/nrneph.2014.102
PMC: PMC5893150
OpenAlex: W1978940943
Cited by: 956
References: 205
Citations by year: 2026: 36 · 2025: 50 · 2024: 67 · 2023: 93 · 2022: 105 · 2021: 109 · 2020: 98 · 2019: 98 · 2018: 93 · 2017: 82 · 2016: 66 · 2015: 46 · 2014: 13
FWCI: 11.08
Type: journal article
Language: en
Open access: green
europepmc.org
Licence: www.springer.com/tdm (tdm)
Locations: Nature Reviews Nephrology (publishedVersion)
PubMed (publishedVersion)
Europe PMC (PubMed Central) (acceptedVersion)
PubMed Central (acceptedVersion)
Funders: National Institutes of Health
Eunice Kennedy Shriver National Institute of Child Health and Human Development (HHSN275201300006C, ZIAHD002400)
Topics: Health Sciences › Medicine › Obstetrics and Gynecology › Pregnancy and preeclampsia studies
Health Sciences › Medicine › Psychiatry and Mental health › Neurological Complications and Syndromes
Life Sciences › Immunology and Microbiology › Immunology › Reproductive System and Pregnancy
Keywords: preeclampsia, pathophysiology, angiogenic imbalance, anti-angiogenic factors, endothelial dysfunction, placenta, oxidative stress, endoplasmic reticulum stress, platelet activation, thrombin, intravascular inflammation, proteinuria, hypertension in pregnancy, maternal morbidity, perinatal mortality, fetal growth restriction, fetal death, spontaneous preterm labor, perivillous fibrin deposition, genetic susceptibility, environmental risk factors
MeSH terms: Adult, Animals, Female, Fetal Growth Retardation, Humans, Hypertension, Kidney, Pre-Eclampsia, Pregnancy, Pregnancy Trimester, Second, Proteinuria, Uterus, Platelet Activation, Oxidative Stress, Vascular Endothelial Growth Factor Receptor-1, Endothelial Cells, Receptor, Angiotensin, Type 1, Endoplasmic Reticulum Stress

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Pre-eclampsia part 1: current understanding of its pathophysiology

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