While increased levels of the anti-angiogenic factors, such as sFlt1 (soluble fms-like tyrosine kinase 1), and decreased levels of angiogenic factors, such as placenta growth factor (PlGF) and vascular endothelial growth factor (VEGF), are associated with hypertension and proteinuria and, subsequently, the development of PE [26], increasing evidence suggests that the terminal complement proteins C5a and C5b-9 are also involved in this process. This evidence concerns the gene C5 and hypertensive disorder.