Preeclampsia is characterized by new-onset hypertension and proteinuria after 20 weeks of gestation. However, this condition extends far beyond hypertension and proteinuria, representing a systemic and complex syndrome that affects all organ systems. It occurs in approximately 5–7% of all pregnancies. Although the exact etiology of preeclampsia remains unclear, it is believed to result from widespread endothelial damage due to inadequate trophoblastic invasion or defective placentation. Severe preeclampsia and eclampsia are among the leading causes of maternal and fetal morbidity and mortality. Optimal management of these cases involves hospitalization in well-equipped centers, prevention of convulsions, control of blood pressure, prevention of hypoxia, and timely delivery.

Most clinical manifestations are associated with endothelial dysfunction. A variety of genetic, immunological, and environmental factors are implicated in its pathogenesis. Soluble fms-like tyrosine kinase-1 (sFlt-1), which is related to decreased serum levels of vascular endothelial growth factor (VEGF) and placental growth factor (PlGF), plays a role as an antiangiogenic factor in the pathogenesis of preeclampsia. The characteristic glomerular lesion observed in preeclampsia is glomerular endotheliosis, which is thought to result from reduced VEGF levels. Emerging data on the pathophysiological mechanisms of preeclampsia suggest that antiangiogenic factors may play a potential role in both screening and treatment.