Preeclampsia (PE) is
one of the main causes of maternal and fetal
morbidity and mortality in the world, causing
nearly 40% of births delivered before 35
weeks of gestation. PE begins with inadequate
trophoblast invasion early in pregnancy, which
produces an increase in oxidative stress
contributing to the development of systemic
endothelial dysfunction in the later phases of
the disease, leading to the characteristic
clinical manifestation of PE. Numerous methods
have been used to predict the onset of PE with
different degrees of efficiency. These methods
have used fetal/placental and maternal markers
in different stages of pregnancy. From an
epidemiological point of view, many studies have
shown that PE is a disease with a strong
familiar predisposition, which also varies
according to geographical, socioeconomic, and
racial features, and this information can be
used in the prediction process. Large amounts of
research have shown a genetic association with a
multifactorial polygenic inheritance in the
development of this disease. Many biological
candidate genes and polymorphisms have been
examined in their relation with PE. We will
discuss the most important of them, grouped
by the different pathogenic mechanisms involved
in PE.