What is the pathophysiology of preeclampsia?
The initiating factor in preeclampsia is incomplete remodeling of uterine spiral arteries, which results in placental ischemia.
The ischemic placenta produces high levels of the antiangiogenic factors, soluble Fms-like tyrosine kinase (sFlt1) and soluble endoglin which are released into the circulation. Levels of placental growth factor (PlGF) and vascular endothelial growth factor (VEGF) are low. sFlt1 antagonizes the angiogenic activity of VEGF and PlGF, causing diffuse vasoconstriction and glomerular endothelial damage.
Therapies targeting antiangiogenic factors to treat preeclampsia are an ongoing area of investigation.
A different pathogenesis has been proposed for late-onset preeclampsia (more than 34 weeks gestation). In late preeclampsia, the problem may be maternal endothelial dysfunction in response to oxidative stress in the placenta.
