Gestational hypertension (GH) and preeclampsia (PE) are characterized by an imbalance in angiogenic factors. However, the relationship among these factors with the severity of hypertensive disorders of pregnancy (HDP) and adverse outcomes are not fully elucidated. We examined whether these biomarkers are related with the severity of HDP and adverse outcomes.Using a cross-sectional design, serum concentrations of placental growth factor (PlGF), soluble fms-like tyrosine kinase-1 (sFlt-1), and soluble endoglin were determined in 764 pregnant women: 75 healthy pregnant, 83 with mild GH (mGH), 105 with severe GH (sGH), 122 with mild PE (mPE), and 379 with severe PE (sPE).All angiogenic factors’ concentrations were significantly different (P ≤ 0.041) in HDP than in healthy pregnancy. In addition, these factors were markedly different in sPE than in mPE, sGH, or mGH (P ≤ 0.027) and in patients with sGH that in those with mPE or mGH (P < 0.05). As compared to mGH and mPE, patients with sGH and sPE had higher rates of both preterm delivery at <34 weeks of gestation and small-for-gestational age infants. Moreover, patients with sPE had higher rates of adverse maternal outcomes (P < 0.001) when compared to patients with mGH, sGH, or mPE. In all cases, levels of sFlt-1/PlGF ratio were significantly higher in patients with sGH and sPE who had adverse perinatal and maternal outcomes than in those with sGH and sPE who did not (P ≤ 0.016).Circulating concentrations of angiogenic factors appear to be suitable markers to assess the severity of GH and PE, and adverse outcomes.

Preeclampsia is characterized by an increased sensitivity to angiotensin II (Ang II). We herein assessed whether serum Ang II levels measured by a new developed bioassay are associated with preeclampsia, its severity, and the risk for developing this disease.Using a cross-sectional design, we studied 90 pregnant women (30 healthy pregnant and 60 with preeclampsia [30 with- and 30 without severe features]). We also used a nested case-control study with 30 women who eventually developed preeclampsia and 31 normotensive controls. Serum samples were collected at diagnosis of preeclampsia or at 4-week intervals (from weeks 12th to 36th). Ang II was measured using a bioassay.At diagnosis of preeclampsia, serum Ang II concentrations were significantly lower in preeclampsia without and with severe features (P = .001 and P < .001, respectively) than in healthy pregnancy. In addition, Ang II was different in preeclampsia with severe features than in those without severe features (P = .048). Women who subsequently developed preeclampsia had lower Ang II levels than women with normal pregnancies, and these changes became significant at 24 weeks onward. The risk to developing preeclampsia was higher among women with Ang II concentration values in the lowest quartile of the control distribution from 12 weeks onward (odds ratio ranging from 3.8 [95% CI 1.3–11.1] to 6.5 [95% CI 1.6–26.9]).We concluded that concentrations of Ang II are markedly diminished at diagnosis of preeclampsia and are closely associated with the severity of disease. Changes in circulating levels of Ang II precede the clinical presentation of preeclampsia.