Preeclampsia is a syndrome diagnosed by hypertension and proteinuria after 20 weeks of gestation; it affects 5–10% of all pregnancies and remains a leading cause of maternal and fetal morbidity and mortality. Based on clinical presentation, preeclampsia is considered as a late pregnancy disorder, but the molecular events leading to its onset seem to occur early in pregnancy. The early phase of the disease is characterized by suboptimal placentation and hemodynamic maladaptation to the pregnancy while at later stages generalized vascular dysfunction leading to clinical syndrome of preeclampsia, Maternal symptoms of preeclampsia are considered consequences of placental pathology associated with poor placental perfusion, inflammation and ischemia / hypoxia,trophoblast damageand activation of complement pathways either classical or alternative pathway.the activation of the complement system plays an important role both in maintaining normal pregnancy and in the pathogenesis of pre‐eclampsia, activation of both classical and alternative pathways plays an important role in cleaning up the numerous trophoblastic cell fragments formed during the placental establishment process. If the complement system is over activated, however, the activating complement component C3a and C4a can activate a maternal systemic inflammatory response, leading to the corresponding manifestations of pre‐eclampsia