Relationship between serum uric acid, nocturnal hypertension and risk for preeclampsia in high-risk pregnancies.

To analyze the possible association between serum uric acid (SUA) and nocturnal hypertension and to evaluate the ability of these variables (alone or in combination) to predict preeclampsia (PE) we conducted a historical cohort study in 532 high-risk pregnancies. Women were divided according to SUA values and nocturnal blood pressure (BP) into four groups: 1- normal SUA and nocturnal normotension; 2- high SUA and nocturnal normotension; 3- normal SUA and nocturnal hypertension and 4- high SUA and nocturnal hypertension. High SUA was defined by the top quartile values and nocturnal hypertension as BP ≥ 120/70 mmHg, using ambulatory blood pressure monitoring (ABPM), during nocturnal rest. Risks for PE were compared using logistic regression. SUA had a weak but significant correlation with daytime systolic ABPM (r = 0.11, p = 0.014), daytime diastolic ABPM (r = 0.13, p = 0.004), nighttime systolic ABPM (r = 0.16, p < 0.001) and nighttime diastolic ABPM (r = 0.18, p < 0.001). Also, all ABPM values were higher in women with high SUA. The absolute risk of PE increased through groups: 6.5%, 13.1%, 31.2%, and 47.9% for groups 1, 2, 3, and 4, respectively, p < 0.001. Compared with Group 1, Group 3 (OR 6.29 95%CI 3.41-11.60), but not Group 2 (OR 2.15 95%CI 0.88-5.24), had statistically significant higher risk for PE. Group 4 (women with both, high SUA and nocturnal hypertension) had the highest risk (OR 13.11 95%CI 6.69-25.70). Risks remained statistically significant after the adjustment for relevant variables. In conclusion, the combination of SUA > 4 mg/dL and nocturnal BP > 120/70 mmHg implies a very high risk to developed PE.

Circulating angiotensin-(1-7) is decreased in patients with isolated nocturnal hypertension.

Isolated nocturnal hypertension (INHT), defined as nighttime elevated blood pressure (BP) with normal daytime BP assessed by ambulatory BP monitoring, is associated with higher cardiovascular morbidity and mortality. We hypothesized that an alteration in the circulating renin-angiotensin system (RAS) contributes to INHT development. We examined circulating levels of angiotensin (Ang) (1-7) and Ang II and ACE2 activity in 26 patients that met the INHT criteria, out of 50 that were referred for BP evaluation (62% women, 45 ±â€Š16 years old). Those with INHT were older, had a higher BMI, lower circulating Ang-(1-7) (P = 0.002) and Ang II levels (P = 0.02) and no change in ACE2 activity compared to those normotensives. Nighttime DBP was significantly correlated with Ang-(1-7) and Ang II levels. Logistic regression showed significant association in Ang-(1-7) and Ang II levels with INHT. Our study reveals differences in circulating RAS in individuals with INHT.

Hypertension arising after 20 weeks of gestation: gestational hypertension or masked chronic hypertension?

The objectives of this study were 1-to evaluate the prevalence of masked chronic hypertension in pregnant women classified as gestational hypertension 2-to compare the risks of developing preeclampsia in true gestational hypertension vs those women classified as having gestational hypertension but who had had masked hypertension in the first half of pregnancy. We conducted a cohort study in consecutive high-risk pregnancies who were evaluated before 20 weeks of gestation. Women who developed gestational hypertension (normotension in the office before 20 weeks of gestation and office BP ≥ 140/90 mmHg and/or antihypertensive treatment in the second half of gestation) were divided, according to an ABPM performed before 20 weeks of pregnancy, in two subgroups: subgroup 1-if their ABPM was normal, and subgroup 2-if they had masked chronic hypertension. Risks for preeclampsia (PE) were estimated and compared with normotensive women. Before 20 weeks of gestation, 227 women were evaluated (age 32 ± 6 years, median gestation age 15 weeks); 67 had chronic hypertension (29.5%). Of the remaining 160, 39 developed gestational hypertension (16 in subgroup 1 and 23 insubgroup 2. Compared with normotensive pregnant women, subgroup 1 of women with gestational hypertension did not increase the risk of developing PE (OR = 0.76, 95% CI = 0.16-6.65). Conversely, subgroup 2 of gestational hypertension increased the risk of PE more than 4 times (0R = 4.47 CI = 1.16-12.63). Risk estimation did not change substantially after the adjustment for multiple possible confounders. In conclusion, the59% of women initially diagnosed as gestational hypertensive according to current recommendations had masked chronic hypertension and a very high risk of developing PE.

Uncontrolled and masked uncontrolled blood pressure in treated pregnant women with chronic hypertension and risk for preeclampsia/eclampsia.

To analyze the relationship between the level of BP achieved with treatment and the risk for development of preeclampsia/eclampsia (PE), we conducted a historical cohort study on 149 consecutive pregnant women with treated chronic hypertension, evaluated between January 1, 2016, and November 31, 2022. According to office BP readings and ambulatory blood pressure monitoring (ABPM) performed after 20 weeks of gestation, the cohort was classified in controlled hypertension, white-coat uncontrolled hypertension, masked uncontrolled hypertension and sustained hypertension. Risks for the development of PE were estimated using logistic regression. One hundred and twenty-four pregnant women with a control BP evaluation were included in this analysis. The rates of PE were 19.4%, 27.3%, 44.8% and 47.1% for controlled, white-coat uncontrolled, masked uncontrolled and sustained uncontrolled hypertension, respectively. Compared with women with controlled hypertension, the relative risk for PE increased markedly in women with sustained uncontrolled (OR 3.69, 95% CI, 1.19-11.45) and masked uncontrolled (OR 3.38, 95% CI, 1.30-11.45) hypertension, but not in those with white-coat uncontrolled (OR 1.56 95% CI, 0.36-6.70); adjustment for covariates did not modify the results. Each mmHg higher of systolic and diastolic daytime ABPM increased the relative risk for PE ~4% and ~5%, respectively. Each mmHg higher of systolic and diastolic nocturnal BP increased the risk ~5% and ~6%, respectively. When these risks were adjusted for ABPM values in opposite periods of the day, only nocturnal ABPM remained as a significant predictor. In conclusion, masked uncontrolled hypertension implies a substantial risk for the development of PE, comparable to those of sustained uncontrolled. The presence of nocturnal hypertension seems important.