The pathogenesis of pre-eclampsia is biphasic. The first phase is characterised by insufficient placentation and the second phase by an increased placental release of 2 anti-angiogenic factors, namely, soluble fms-like tyrosine kinase 1 (sFlt-1) and soluble endoglin (sEng). Within maternal circulation, sFlt-1 and sEng inhibit the effects of vascular endothelial growth factor (VEGF) and transforming growth factor β (TGFβ). This results in endothelial cell activation and inflammation, and eventually leads to the clinical syndrome of pre-eclampsia. The rise in plasma concentrations of sFlt-1 and sEng precedes the development of pre-eclampsia with 6-8 weeks. Whether elevations in the plasma concentrations of sFlt and sEng, combined with a decrease in placental growth factor concentrations, can be utilised as a predictor for pre-eclampsia is currently under investigation.