Preeclampsia is a pregnancy complication that can be life threatening for both mother and baby when clinical findings are severe. The pathogenesis of the disease, in which the main findings are hypertension and proteinuria, is not precisely understood, but abnormal placenta formation could explain the mechanism of the clinical findings. Because of this abnormal placentation, the ischemic plasenta secretes sFLT-1 (soluble fms-like tirozine kinase-1; synonym, sVEGFR-1, soluble vascular endothelial growth factor receptor-1) and sEng (soluble endoglin), which binds to VEGF (vascular endothelial growth factor); the consequent low levels of VEGF may, along with other factors such as genetics, explain the clinical findings of preeclampsia. Babies born to pregnancies where preeclampsia is present may have complications due to prematurity and intrauterine growth restriction. The main problem for the fetus or the newborn is uteroplacental ischemia. Plasental ischemia and infarct may cause damaged decidual cells to bleed. Ablatio placenta can bring on fetal death if the bleeding occurs in the uteroplacental space. Recent studies report that not only uteroplacental insufficiency, but also the factors responsible for the pathogenesis of preeclampsia play a part in the neonatal complications. Understanding the mechanisms of the clinical findings of preeclampsia throws light on possible treatment options. Animal experiments have guided researchers with regard to reduction of sFLT-1 expression and administration of VEGF for preventing or treating preeclampsia.

Keywords: <i>intrauterin büyüme kısıtlılığı, plasenta, preeklampsia, sENG, sFLT- 1, sVEGFR-1, VEGF, yenidoğan.</i>