Abstract
Preeclampsia is a serious complication of pregnancy where it affects 5–8% of all pregnancies. It increases the morbidity and mortality of both the fetus and pregnant woman, especially in developing countries. It deleteriously affects several vital organs, including the kidneys, liver, brain, and lung. Although, the pathogenesis of preeclampsia has not yet been fully understood, growing evidence suggests that aberrations in the angiogenic factors levels and coagulopathy are responsible for the clinical manifestations of the disease. The common nominator of tissue damage of all these target organs is endothelial injury, which impedes their normal function. At the renal level, glomerular endothelial injury leads to the development of maternal proteinuria. Actually, peripheral vasoconstriction secondary to maternal systemic inflammation and endothelial cell activation is sufficient for the development of preeclampsia-induced hypertension. Similarly, preeclampsia can cause hepatic and neurologic dysfunction due to vascular damage and/or hypertension. Obviously, preeclampsia adversely affects various organs, however it is not yet clear whether pre-eclampsia per se adversely affects various organs or whether it exposes underlying genetic predispositions to cardiovascular disease that manifest in later life. The current review summarizes recent development in the pathogenesis of preeclampsia with special focus on novel diagnostic biomarkers and their relevance to potential therapeutic options for this disease state. Specifically, the review highlights the renal manifestations of the disease with emphasis on the involvement of angiogenic factors in vascular injury and on how restoration of the angiogenic balance affects renal and cardiovascular outcome of Preeclamptic women.
Highlights
Preeclampsia (PE) is a profound complication of pregnancy, where it affects 3–8% of all pregnancies and dramatically increases the risk of all-cause mortality, especially in women who experienced early, severe, preterm episode (Backes et al, 2011; Jim and Karumanchi, 2017)
pump inhibitors (PPIs) used by pregnant women (430 in number) was associated with decrease in sFlt-1 (Saleh et al, 2017). Their plasma endoglin and ET-1 levels were lower while sFlt-1 levels correlated positively with both. These findings suggest that PPI may bear therapeutic potential for preeclampsia, prospective trials are still warranted
The abnormal angiogenic ratios are subsequent to the impaired placentation, and not the cause of it, as there is no evidence that sFLT affects trophoblast invasion
Summary
Preeclampsia (PE) is a profound complication of pregnancy, where it affects 3–8% of all pregnancies and dramatically increases the risk of all-cause mortality, especially in women who experienced early, severe, preterm episode (Backes et al, 2011; Jim and Karumanchi, 2017). The definition of preeclampsia was revisited as the mechanisms underlying the disease were dramatically evolved Concerning the former, several leading groups have challenged the half century old classic definition of preeclampsia, namely, de novo hypertension, new onset of proteinuria and liver dysfunction after mid pregnancy, motivated by the discovery of additional biomarkers of preeclampsia (Tjoa et al, 2007; Staff et al, 2013; Palomaki et al, 2015; Baltajian et al, 2016). In this context, several studies have suggested to modernize the definition by incorporating key biomarkers of either placental or vascular origins, including placenta growth factor (PlGF) and antiangiogenic factors
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