Preeclampsia/eclampsia is a major cause of maternal and fetal morbidity worldwide. Although the etiology of preeclampsia is still unclear, the clinical phenotypes of preeclampsia have been demonstrated to be related to high circulating levels of anti-angiogenic proteins secreted by the placenta such as soluble Fms-like tyrosine kinase 1 (sFlt1) and soluble endoglin. Because, alterations in circulating sFlt1 and soluble endoglin precede the onset of clinical disease, these factors may be useful to screen or identify patients at risk for preeclampsia. Investigations are currently underway of various pharmacologic agents to counteract the effects of sFlt1 and/or sEng as a potential treatment for preeclampsia. Recently several isoforms of sFlt1 have been described, such as sFlt1-14 which is expressed only in primates, and is thought to be the primary isoform produced by the placenta in preeclamptic subjects. Although several novel pathways have been proposed to play key roles in inducing sFlt1 production, the exact role of these pathways in human preeclampsia is still not known. Women with a history of preeclampsia have an increased risk of hypertension, and cardiovascular and renal disease. Whether these long-term observations are due to persistent and subtle endothelial damage as result of preeclampsia, or simply reflect the consequences of the vascular risk factors which are more common in these women remains unknown.