Abstract
Preeclampsia is a common disorder of human pregnancy and is a leading cause of maternal and neonatal death world-wide. The disease is polymorphic, with involvement of the placenta, maternal vasculature, central nervous system, coagulation cascade, liver and kidney. Preeclampsia is also associated with an increased incidence of fetal intrauterine growth restriction (IUGR). Often, the only treatment option is delivery with consequent fetal prematurity. The clinical markers of this disorder include hypertension and proteinuria, which reverse after delivery. Hypertension is a result of the disease and is rarely of pathogenic importance. When accompanied by convulsions the syndrome is termed eclampsia (derived from the Greek eklampsis or “sudden flashing”). A primary clinical goal is to prevent progression to this deadly complication. The incidence of preeclampsia is between 5 and 10% of pregnancies and there is no evidence that this has changed appreciably during the last century. Despite the lack of progress from a practical standpoint, new insights into the aetiology and pathogenesis of preeclampsia continue to arise.