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Antagonizing vasodilation has been considered one of the potential mechanisms underlying the pathophysiology of preeclampsia. Phosphodiesterases hydrolyze cGMP, interfering with the action of nitric oxide on vascular smooth muscle, thus causing vasoconstriction. We hypothesize that the phosphodiesterases in maternal plasma, phosphodiesterase-5 in particular, may be linked to clinical manifestations in preeclampsia syndrome.

Objectives Postpartum stratification of cardiovascular risk for women with pregnancies complicated by pre-eclampsia is challenging. Our aim was to identify potential clinical and biomarker predictors of future cardiovascular risk at six weeks postpartum in women with hypertensive pregnancies. Study design: Prospective longitudinal cohort Main outcome measures Ten year- Framingham cardiovascular risk scores were calculated for 477 women (94 with gestational hypertension, 288 with pre-eclampsia, 30 with superimposed pre-eclampsia, 51 with chronic hypertension, 14 women with uncomplicated pregnancies). B-type natriuretic peptide (BNP), neutrophil gelatinase–associated lipocalin (NGAL) and placental growth factor (PlGF) were quantified at six weeks postpartum. Results Framingham cardiovascular risk scores were not higher in women with pregnancies complicated by pre-eclampsia than healthy controls, nor were scores higher in women with pre-existing chronic hypertension complicated with superimposed pre-eclampsia compared with those without superimposed pre-eclampsia. Women with gestational hypertension had higher risk scores than women with pre-eclampsia and healthy controls. Established risk factors of cardiovascular disease including diastolic blood pressure and previously diagnosed chronic hypertension were associated with higher scores, and African ethnicity, parity and estimated glomerular filtration rate also were independently associated with higher Framingham risk scores at six weeks postpartum. PlGF, BNP and NGAL concentrations were not associated with Framingham cardiovascular risk scores after adjustment for independent variables. Conclusions A history of pre-eclampsia or superimposed pre-eclampsia in most recent pregnancy was not associated with elevated Framingham risk score at six weeks postpartum. Established clinical predictors may enable risk stratification at six weeks postpartum, which are not enhanced by the biomarkers included in this study.

Introduction - Singling out high-risk patients from the diverse hypertensive disorders of pregnancy, and not only preeclampsia, is a challenge for clinicians. The fullPIERS model is a simple and low-cost evaluation instrument using clinical variables to stratify the adverse outcomes probability of pregnant women with high-risk preeclampsia. Placental growth factor (PlGF) levels are reduced in preeclampsia and are increasingly being used as a biomarker in the assessment of this disease. Objectives - The aim of the study is to evaluate the performance of the fullPIERS model and PlGF to predict adverse outcomes in women with hypertensive disorders of pregnancy. Methods - A prospective cohort study carried out at a teaching hospital in Porto Alegre, Brazil enrolling pregnant women admitted with a systolic blood pressure ≥ 140 mmHg and/or a diastolic blood pressure ≥ 90 mmHg from the 20th week of gestation. First 48 hours of admission worst clinical and laboratory data were recorded and the development of adverse maternal and perinatal outcomes scrutinised up to 14 days. Admission maternal plasma PlGF concentrations were measured. Results – A total of 405 women were enrolled. From the 351 women included in the fullPIERS model analysis, 20 (5%) developed at least one of the combined maternal adverse outcomes. The fullPIERS model had poor outcomes discrimination at 48h [AUC 0.639 (95% CI 0.458-0.819)]. At the seventh admission day, the model’s accuracy was even lower [AUC 0.612 (95% CI 0.440-0.783)]; the model’s discriminative ability remained similar [AUC 0.637 (95% CI 0.491-0.783)] at 14 days. Calibration of the fullPIERS model was poor: slope - 0.35 (95% CI 0.08-0.62), intercept -1.13 (95%CI -2.4-0.14). PlGF analysis included 392 women. PlGF < 5th percentile predicted maternal adverse outcomes within 48h in women with gestation < 35 weeks with sensitivity of 0.80, NPV of 0.98 and AUC ROC of 0.672 (CI 95%0.5-0.9). The threshold of

Introduction The fullPIERS model is an instrument of simple evaluation and low-cost that uses clinical variables to stratify pregnant women with preeclampsia at high risk for adverse outcomes. However, differentiating high-risk patients amongst the variety presentations of hypertension disorders of pregnancy (HDP), not only preeclampsia, represents a daily challenge for obstetricians. Objectives The aim of this study is to evaluate the use of the fullPIERS model as a predictor of maternal and fetal adverse outcomes in women with hypertensive disorders of pregnancy. Methods This is a prospective cohort ongoing at the obstetric unit of a teaching hospital in Porto Alegre, Brazil. Pregnant women, after 20 weeks of gestation, admitted to the hospital with systolic blood pressure ⩾ 140 and/or diastolic blood pressure ⩾ 90 mmHg were enrolled. Women in active labor at the moment of hospital admission were excluded. The worst clinical and laboratory data from the first 48 hours after admission were recorded. Development of maternal and perinatal outcomes was observed for 14 days. Classification into HDP categories (gestational hypertension, preeclampsia, chronic hypertension and chronic hypertension with superimposed preeclampsia) was completed after delivery. Results • Until this moment, seventy-nine women were included to the study. Thirteen (16.5%) with gestational hypertension, 44 (55.5%) with preeclampsia, 11 (14%) with superimposed preeclampsia and 11 (14%) with chronic hypertension. • Thirty three (42%) women had at least one adverse outcome. Elevated liver enzymes was the most common adverse outcome, occurring in 28 (35%) women. • The group with gestational hypertension had a significant lower incidence of adverse maternal outcomes (2 cases, 15%) when compared to preeclampsia (20 cases, 45.5%) (p 0.05) and superimposed preeclampsia patients (6 cases, 54.5%) (p 0.05). There were no differences comparing development of adverse outcomes between preeclampsia and superimposed preeclampsia groups, or comparing the chronic hypertensive group (5 cases, 45.5%) with any of the other groups. • Twelve (15%) newborns were admitted to intensive care unit and four (5%) neonatal deaths occurred. Women with preeclampsia and superimposed preeclampsia had more perinatal adverse outcomes when compared to other groups (p 0.009). • The fullPIERS model did not demonstrate association with the development of maternal adverse outcomes during the 14 days of follow-up. On the other hand, fullPIERS model predicted adverse fetal outcomes within 14 day of eligibility (AUC ROC 0.73, 95% CI 0.56-0.89). The classification accuracy of fullPIERS was fair. Using a predicted probability of 0.16 as a threshold, fullPIERS obtained a specificity of 80% and a negative predictive value of 90%, whereas correctly classified 54% of women who subsequently had events as being at high risk. Conclusions In our study, fullPIERS model could not predict maternal adverse outcomes within 14 days of hospital admission in women with different categories of HDP. However, we demonstrated that fullPIERS had a reasonable discrimination predicting fetal adverse outcomes in the same period. The main limitation of this study is the small sample size, especially in view of the broad spectrum of pregnant women with elevated blood pressure included. Nonetheless, the elevated rate of adverse outcomes in our sample corroborates to the need for studies that can be generalized to the women with HDP presenting with different features at obstetric units.

Objective:Characterize a group of women that developed eclampsia and to compare it with a group that had preeclampsia focusing in maternal serum uric acid and proteinuria-to-creatininuria ratio.Design and method:The records of patients delivered at Hospital Sao Lucas/Pontificia Universidade Catolica

Introduction Systemic renin–angiotensin–aldosterone system (RAAS) activity is augmented in non-pregnant women with chronic kidney disease (CKD) and chronic hypertension (CHT), but its activity in pregnancy and superimposed pre-eclampsia is poorly understood. Objectives (i) To compare longitudinal changes in plasma renin and angiotensinogen concentrations in pregnant women with CKD and CHT with healthy controls. (ii) To compare differences in plasma renin and angiotensinogen concentrations in pregnant women with CKD and CHT with and without superimposed pre-eclampsia and women with pre-eclampsia without pre-existing disease. Methods Plasma renin activity and angiotensinogen were quantified in samples from women with CKD or CHT, women with pre-eclampsia without pre-existing disease and healthy controls recruited to a longitudinal prospective cohort study at two London Academic Health Centers. Demographics and pregnancy outcomes were extracted from patient records. RAAS component concentrations were compared across gestational ages using repeated measures analysis. Results One hundred and ninety-five women were recruited (CKD=80; Primary CHT=31; Pre-eclampsia without pre-existing disease=19; Healthy controls=65). Eighteen women with CKD (22.5%) and 10 women (32.3%) with primary CHT developed superimposed pre-eclampsia. Plasma renin activity was lower in women with CKD or CHT with compared to healthy controls at all gestational time points ( p p 0.003) or healthy controls ( p Conclusion Women with CKD or CHT have suppressed plasma renin activity during pregnancy compared with healthy controls. After diagnosis of superimposed pre-eclampsia women with CKD or CHT have lower plasma renin than women without superimposed pre-eclampsia, but there are no differences between women with pre-eclampsia and superimposed pre-eclampsia, suggestive of a common pathophysiological pathway.

Introduction Hypertensive disorders of pregnancy (HDP) occur in 6–10% of all pregnancies. A significant proportion of previously normotensive women persist with elevated blood pressure 12 weeks postpartum. Investigation on factors involved in the persistence of hypertension is of critical importance to provide quality health care for those women. The aim of our study is to identify factors involved in the persistence of hypertension at 12 weeks after pregnancies complicated by HDP. Methods We conducted a case-control study nested in a prospective cohort of outpatient women who had HDP at a teaching hospital in Porto Alegre, RS. At first visit, all women informed socio-demographic characteristics, medical and pregnancy histories. At follow-up visits we collected information on use of antihypertensive medication, blood pressure, urinary and serum analysis. Results We selected 99 women in the cohort with no pre-existing hypertension and that were followed until 12 weeks postpartum. Hypertensive women after 12 weeks from delivery were considered cases (n = 56) and normotensive women after 12 weeks were labelled controls (n = 43). We developed a risk prediction model with independent variables for persistent hypertension after pregnancy. Our results showed that both blood pressure and use of antihypertensive medication were significantly different at first visit. Mean systolic and diastolic blood pressure were, respectively, 138.6 (20.6) mmHg and 91.9 (12.3) mmHg for the hypertensive group and 117.9 (12) mmHg and 78.4 (8.9) mmHg for controls (p 0.001). Maternal age was significantly higher in the hypertensive group. Gestational outcomes and biochemical parameters were similar between groups. Gestational age at delivery, maternal age and both systolic and diastolic blood pressures at first visit were independent variables chosen to compose a risk model with an area under the ROC of 0.896 (95% CI 0.819-0.972) to predict persistent hypertension after pregnancy. Conclusion Gestational age at delivery, maternal age and blood pressure were identified as important factors involved in persistent hypertension 12 weeks after pregnancies complicated by HDP. We believe that prospective studies with larger population are needed to access the value of a risk model to predict, at first visit postpartum, which women have increased chance to become chronically hypertensive.