Pre-eclampsia is a multisystemic disorder characterized by new-onset hypertension and proteinuria after 20 weeks of gestation, or hypertension with systemic disease in the absence of proteinuria. It is a leading cause of maternal and perinatal morbidity and mortality. The placenta plays a central role in its development, with pathogenetic mechanisms including defective placentation, oxidative and endoplasmic reticulum stress, autoantibodies to the angiotensin II type 1 receptor, platelet and thrombin activation, intravascular inflammation, endothelial dysfunction, and an antiangiogenic state. An imbalance in angiogenesis is a key factor, though not specific to pre-eclampsia, as it also occurs in other conditions like intrauterine growth restriction and fetal death. The severity and timing of this imbalance, along with maternal susceptibility, influence the clinical presentation. Risk factors include young age, first pregnancy, genetic predisposition, and immune mechanisms. Diagnosis involves hypertension and proteinuria, though the latter is debated. Pre-eclampsia can present with atypical features like HELLP syndrome. It is classified by gestational age and severity. Pathogenetic mechanisms involve placental ischaemia, transformation of spiral arteries, hypoxia, and trophoblast invasion. Endoplasmic reticulum and oxidative stress, along with antiangiogenic factors like sVEGFR-1 and soluble endoglin, contribute to the disease. Intravascular inflammation, endothelial dysfunction, and thrombin activation further exacerbate the condition. The antiangiogenic state, driven by factors like sVEGFR-1, leads to hypertension and proteinuria. While these mechanisms are not exclusive to pre-eclampsia, their interplay determines the clinical outcomes. The "great obstetrical syndromes" concept highlights the complex interactions between maternal and fetal factors in these conditions.Pre-eclampsia is a multisystemic disorder characterized by new-onset hypertension and proteinuria after 20 weeks of gestation, or hypertension with systemic disease in the absence of proteinuria. It is a leading cause of maternal and perinatal morbidity and mortality. The placenta plays a central role in its development, with pathogenetic mechanisms including defective placentation, oxidative and endoplasmic reticulum stress, autoantibodies to the angiotensin II type 1 receptor, platelet and thrombin activation, intravascular inflammation, endothelial dysfunction, and an antiangiogenic state. An imbalance in angiogenesis is a key factor, though not specific to pre-eclampsia, as it also occurs in other conditions like intrauterine growth restriction and fetal death. The severity and timing of this imbalance, along with maternal susceptibility, influence the clinical presentation. Risk factors include young age, first pregnancy, genetic predisposition, and immune mechanisms. Diagnosis involves hypertension and proteinuria, though the latter is debated. Pre-eclampsia can present with atypical features like HELLP syndrome. It is classified by gestational age and severity. Pathogenetic mechanisms involve placental ischaemia, transformation of spiral arteries, hypoxia, and trophoblast invasion. Endoplasmic reticulum and oxidative stress, along with antiangiogenic factors like sVEGFR-1 and soluble endoglin, contribute to the disease. Intravascular inflammation, endothelial dysfunction, and thrombin activation further exacerbate the condition. The antiangiogenic state, driven by factors like sVEGFR-1, leads to hypertension and proteinuria. While these mechanisms are not exclusive to pre-eclampsia, their interplay determines the clinical outcomes. The "great obstetrical syndromes" concept highlights the complex interactions between maternal and fetal factors in these conditions.