Pre-eclampsia part 1: current understanding of its pathophysiology

Abstract

Diagnosis of pre-eclampsia is based on new-onset hypertension and proteinuria at ≥20 weeks of gestation or, in the absence of proteinuria, hypertension together with evidence of systemic disease Genetic and environmental factors are thought to create conditions leading to defective deep placentation; the injured placenta then releases factors into the maternal circulation that induce pre-eclampsia Pre-eclampsia is characterized by multiple aetiologies and pathogenetic mechanisms, a long subclinical phase, fetal involvement, adaptive clinical manifestations and gene–environment interactions An imbalance between angiogenic and antiangiogenic factors has emerged as a central pathogenetic mechanism in pre-eclampsia An antiangiogenic state can also be observed in conditions other than pre-eclampsia, including intrauterine growth restriction, fetal death, spontaneous preterm labour and maternal floor infarction The severity and timing of the antiangiogenic state, as well as maternal susceptibility, might determine the clinical presentation of pre-eclampsia