sEng levels also increased with gestational age in normotensive pregnancy, indicating that the gestational age was associated with a greater anti-angiogenic profile. This finding is according to previous studies that found higher sEng and lower PlGF levels, and higher/PlGF ratio in older gestational age. Previous studies have demonstrated that sEng is elevated in PE and before the onset of the disease. In contrast to normotensive pregnant women, there is a negative association between sEng levels and gestational age in PE. Accordingly, we found higher sEng levels in PE comparing to normotensive pregnant women that correlated negatively with gestational age. In addition, sEng levels were independently associated with the development of PE, reinforcing the role of sEng in disease pathogenesis. Our data demonstrated that primiparity was also independently associated with pregnancy outcome. In agreement with other studies, we found a tendency of increased sEng levels in early-onset comparing to late-onset PE. Consistent with previous reports, we also found a significant increase of sEng levels in severe PE compared with mild PE. In addition, sEng levels were independently associated with the disease severity. It is well known that blood pressure and protein excretion are increased in preeclamptic women with the severe form of the disease. A recent study has indicated an association between sEng and high blood pressure in pregnancy. In one animal model of PE, the administration of adenovirus encoding sEng produced hypertension, proteinuria and endothelial dysfunction, further amplified by the coadministration of sEng and sFlt1, leading to a severe PE-like disease including HELLP syndrome and fetal growth restriction. In line with these experimental data, we found that systolic blood pressure was positively associated with sEng levels in PE. In accordance to Zhang et al., we showed that sEng and creatinine levels were positively associated in PE. Angiogenesis play a critical role in renal homeostasis, since glomeruli form the functional barrier between the blood and urinary compartment. Genetic studies in mice have revealed an important role of the proangiogenic factors VEGF and PlGF in renal development and vascular health. On the other hand, the anti-angiogenic factors sFlt-1 and sEng have been associated with glomerular damage and proteinuria. Venkatesha et al. showed that proteinuria was modest in sEng-treated rats and severe in sFlt-1treated group, while a nephrotic-range proteinuria was found using both sFlt-1 and sEng. Masuyama et al. demonstrated a tendency of increased proteinuria levels in high sEng group compared to low sEng group. Hepatic function may be significantly altered in PE women, especially in those with the severe form of the disease and this alteration is even more pronounced in HELLP syndrome.