This placental damage results in increased shedding of syncytial micro-particles and other vascular toxins from the foetal unit into the maternal circulation and is thought to contribute to stage where there is generalized endothelial dysfunction.6 Two anti-angiogenic proteins have been identified that are overproduced by the preeclamptic placenta and gain access to the maternal circulation and are the leading candidate molecules responsible for the pre-eclampsia phenotype.