Risk factors
Known risk factors for pre-eclampsia include:
Having never previously given birth
Diabetes mellitus
Kidney disease
Chronic hypertension
Prior history of pre-eclampsia
Family history of pre-eclampsia
Advanced maternal age (>35 years)
Obesity
Antiphospholipid antibody syndrome
Multiple gestation
Having donated a kidney
Having sub-clinical hypothyroidism or thyroid antibodies
Placental abnormalities such as placental ischemia

Pathogenesis
Although much research into mechanism of pre-eclampsia has taken place, its exact pathogenesis remains uncertain. Pre-eclampsia is thought to result from an abnormal placenta, the removal of which ends the disease in most cases. During normal pregnancy, the placenta vascularizes to allow for the exchange of water, gases, and solutes, including nutrients and wastes, between maternal and fetal circulations. Abnormal development of the placenta leads to poor placental perfusion. The placenta of women with pre-eclampsia is abnormal and characterized by poor trophoblastic invasion. It is thought that this results in oxidative stress, hypoxia, and the release of factors that promote endothelial dysfunction, inflammation, and other possible reactions.The clinical manifestations of pre-eclampsia are associated with general endothelial dysfunction, including vasoconstriction and end-organ ischemia. Implicit in this generalized endothelial dysfunction may be an imbalance of angiogenic and anti-angiogenic factors. Both circulating and placental levels of soluble fms-like tyrosine kinase-1 (sFlt-1) are higher in women with pre-eclampsia than in women with normal pregnancy. sFlt-1 is an anti-angiogenic protein that antagonizes vascular endothelial growth factor (VEGF) and placental growth factor (PIGF), both of which are proangiogenic factors.
References
External links
"Glipizide". Drug Information Portal. U.S. National Library of Medicine.