Pre-eclampsia is a multisystemic disorder characterized by new-onset hypertension and proteinuria at ≥20 weeks of gestation. It can also be diagnosed if hypertension is present along with systemic disease signs like thrombocytopenia or elevated liver enzymes. It affects 3–5% of pregnancies and is a leading cause of maternal and perinatal morbidity and mortality. Pre-eclampsia can progress to eclampsia, which involves seizures and affects 2.7–8.2 per 10,000 deliveries. It can lead to severe complications such as cerebral hemorrhage, liver rupture, and acute renal failure. Pre-eclampsia is associated with adverse perinatal outcomes like preterm delivery, intrauterine growth restriction, and fetal death. The placenta is essential for pre-eclampsia development, and it can occur in patients with hydatidiform moles. The traditional view of pre-eclampsia pathogenesis is that an ischemic placenta releases factors into the maternal circulation, causing clinical manifestations. These factors are thought to cause endothelial dysfunction, intravascular inflammation, and activation of the hemostatic system, making pre-eclampsia primarily a vascular disorder. The clinical manifestations result from involvement of multiple organs, including the kidneys, liver, brain, heart, lung, pancreas, and vasculature. Pre-eclampsia is classified as early (<34 weeks) or late (≥34 weeks) based on gestational age at diagnosis or delivery. It can also be classified by severity. The pathogenesis of pre-eclampsia involves placental ischemia, transformation of spiral arteries, hypoxia and trophoblast invasion, endoplasmic reticulum stress, oxidative stress, antibodies to type-1 angiotensin II receptor, intravascular inflammation, endothelial cell activation and dysfunction, platelet and thrombin activation, and an antiangiogenic state. The antiangiogenic state is considered one of the most important factors in pre-eclampsia, with an imbalance of angiogenesis. This imbalance is not specific to pre-eclampsia, as it also occurs in other conditions like intrauterine growth restriction, fetal death, spontaneous preterm labor, and maternal floor infarction. The severity and timing of the angiogenic imbalance, along with maternal susceptibility, might determine the clinical presentation of pre-eclampsia. The diagnosis of pre-eclampsia is based on new-onset hypertension and proteinuria, but some organizations allow diagnosis based on hypertension and systemic involvement. Proteinuria is not always required, as pre-eclampsia might manifest before glomerular capillary endotheliosis becomes severe enough to induce proteinuria. The gold standard for diagnosing proteinuria during pregnancy is a 24-hour urine sample with total protein ≥300 mg. However, this cut-off has notPre-eclampsia is a multisystemic disorder characterized by new-onset hypertension and proteinuria at ≥20 weeks of gestation. It can also be diagnosed if hypertension is present along with systemic disease signs like thrombocytopenia or elevated liver enzymes. It affects 3–5% of pregnancies and is a leading cause of maternal and perinatal morbidity and mortality. Pre-eclampsia can progress to eclampsia, which involves seizures and affects 2.7–8.2 per 10,000 deliveries. It can lead to severe complications such as cerebral hemorrhage, liver rupture, and acute renal failure. Pre-eclampsia is associated with adverse perinatal outcomes like preterm delivery, intrauterine growth restriction, and fetal death. The placenta is essential for pre-eclampsia development, and it can occur in patients with hydatidiform moles. The traditional view of pre-eclampsia pathogenesis is that an ischemic placenta releases factors into the maternal circulation, causing clinical manifestations. These factors are thought to cause endothelial dysfunction, intravascular inflammation, and activation of the hemostatic system, making pre-eclampsia primarily a vascular disorder. The clinical manifestations result from involvement of multiple organs, including the kidneys, liver, brain, heart, lung, pancreas, and vasculature. Pre-eclampsia is classified as early (<34 weeks) or late (≥34 weeks) based on gestational age at diagnosis or delivery. It can also be classified by severity. The pathogenesis of pre-eclampsia involves placental ischemia, transformation of spiral arteries, hypoxia and trophoblast invasion, endoplasmic reticulum stress, oxidative stress, antibodies to type-1 angiotensin II receptor, intravascular inflammation, endothelial cell activation and dysfunction, platelet and thrombin activation, and an antiangiogenic state. The antiangiogenic state is considered one of the most important factors in pre-eclampsia, with an imbalance of angiogenesis. This imbalance is not specific to pre-eclampsia, as it also occurs in other conditions like intrauterine growth restriction, fetal death, spontaneous preterm labor, and maternal floor infarction. The severity and timing of the angiogenic imbalance, along with maternal susceptibility, might determine the clinical presentation of pre-eclampsia. The diagnosis of pre-eclampsia is based on new-onset hypertension and proteinuria, but some organizations allow diagnosis based on hypertension and systemic involvement. Proteinuria is not always required, as pre-eclampsia might manifest before glomerular capillary endotheliosis becomes severe enough to induce proteinuria. The gold standard for diagnosing proteinuria during pregnancy is a 24-hour urine sample with total protein ≥300 mg. However, this cut-off has not