Elevated sVEGFR-1 concentrations at 16-20 wk gestation precede the clinical manifestations of preeclampsia. By neutralizing VEGF, sVEGFR-1 may contribute to inadequate placental vascularization.

Maternal serum Ang-2 concentrations are increased prior to preeclampsia. High concentrations of both Ang-2 and sVEGFR-1 indicate subsequent disease.

The concentrations of endostatin in maternal serum at 16-20 weeks' of gestation are associated with an increased risk of pre-eclampsia but not IUGR.

The disappearance of endogenous sVEGFR-1 after pregnancy is biphasic, and it is associated with a simultaneous increase in free VEGF concentrations.

One cause of unexplained infertility may be unbalanced secretion of sVEGFR-1 with concomitant changes in free VEGF during the transition from the follicular to the luteal phase. This aberration may be related to impaired implantation.