Abstract

Preeclampsia is one of the most frequently encountered hypertensive complication of pregnancy that affect ≈ 5% of pregnant women worldwide.1 It is often characterized by new onset of hypertension and proteinuria, usually during the last trimester of pregnancy, and is commonly associated with edema and hyperuricemia. Preeclampsia occurs only in the presence of the placenta, even when there is no fetus (as in hydatidiform mole) and usually remits when the placenta is delivered. The placenta in preeclampsia is often abnormal, with evidence of hypoperfusion and ischemia. The renal biopsy and autopsy studies from preeclamptic patients showed renal glomerular endotheliosis, a unique form of microvascular endothelial injury that is described as the classic lesion of this disorder.2,3 Besides affecting kidneys, preeclampsia can affect the liver, hematologic system leading to hemolysis and disseminated intravascular coagulation, brain resulting in seizures (eclampsia), renal failure, abruption, fetal growth restriction and in certain cases fetal and maternal death. Preeclampsia remains a major cause of maternal and fetal morbidity and mortality worldwide.4 Because of a general lack of access to advanced pre- and postnatal care, most of these deaths occur in the developing world. Preeclampsia is about twice as common in first pregnancies as in multigravidas. Other predisposing factors include pre-existing hypertension, chronic renal disease, obesity, diabetes mellitus, thrombophilias, trisomy 13, and multiple gestations.5,6 It occurs more frequently in women whose mothers had preeclampsia and in women whose fathers were products of a preeclamptic pregnancy.7 The incidence of preeclampsia is higher in women who live in high altitudes, suggesting that hypoxia may contribute to the development of the syndrome.8 In vitro fertilization has also emerged as an important risk factor for preeclampsia.9 Although none of these risk factors is fully understood, they have provided insights into …

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