Preeclampsia is a serious medical condition which affects approximately 5% of pregnant women. Although preeclampsia is not usually fatal, it is characterized by hypertension, proteinuria, and edema. Complications of preeclampsia can also include seizures, stroke, and kidney and liver failure. Researchers have hypothesized that preeclampsia results from an imbalance of angiogenic factors and studies show that serum, plasma, and urine PlGF levels decrease significantly in women with preeclampsia and/or those who subsequently develop the disorder.
This common and potentially life-threatening complication of pregnancy increasingly appears to be caused by placental insufficiency. It has been shown that increases in the soluble form of endoglin are exaggerated during and, significantly, prior to the onset of preeclampsia symptoms. Endoglin/CD105 is a transmembrane co-receptor that facilitates the binding of TGF-beta 1 or TGF-beta 3 to TGF-beta RII and the recruitment of the type I receptor ALK-1. Endoglin expression is upregulated in endothelial cells and syncytiotrophoblasts during development of the placenta in early pregnancy. Significantly, mild preeclampsia, severe preeclampsia, and HELLP syndrome (hemolysis, elevated liver enzymes, low platelets) are accompanied by a further three-, five-, and ten-fold increase in circulating endoglin, respectively. Serum or plasma placental growth factor (PlGF) and soluble VEGF R1 (sVEGF R1) also increase during normal pregnancy. However, in preeclampsia, the circulating PlGF increase is attenuated while increases in both sVEGF R1 and endoglin are exaggerated.