Aldosterone, Salt, and Potassium Intakes as Predictors of Pregnancy Outcome, Including Preeclampsia
Aldosterone, Salt, and Potassium Intakes as Predictors of Pregnancy Outcome, Including Preeclampsia
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DOI：
10.1161/hypertensionaha.119.12924
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发表时间：
2019-08-01
期刊：
影响因子：
8.3
通讯作者：
Jensen, Boye L.
中科院分区：
文献类型：
--
作者：
Birukov, Anna;Andersen, Louise Bjorkholt;Jensen, Boye L.
正常妊娠妇女血浆中的盐皮质激素醛固酮与肾素、血管紧张素Ⅱ一起升高，在生理性血浆容量扩张中起关键作用。在小鼠中，醛固酮通过促进胎盘生长因子(PlGF)的表达和滋养层细胞的增殖来促进最佳的胎儿发育。在先兆子痫中，醛固酮的抑制和胎盘发育受损是一致的。我们假设，醛固酮独立地影响人类的胎盘和出生体重，高钠低钾摄入会对这种关系产生不利影响。我们分析了丹麦基于人群的纵向队列研究欧登塞儿童队列的569名孕妇从妊娠29周开始的24小时尿液和血浆样本。血浆和尿醛固酮测定采用ELISA法，钠、钾排泄量测定采用火焰光度计法。多因素分析和COX回归分析评估了醛固酮水平和钠、钾摄入量的预测值。主要结果是胎盘重量和出生体重。次要结果是先兆子痫。孕29周尿醛固酮排泄量独立影响胎盘和新生儿体重(调整后的β系数分别为24.50[9.66-39.35]和9.59[4.57-14.61])。醛固酮水平与先兆子痫的发生率无关。盐摄入量6g/d与先兆子痫的发生相关(风险比[95%CI]，5.68[1.51-21.36])。在妊娠29周，尿醛固酮排泄量是胎盘和出生体重的独立预测因子。高盐摄入量是先兆子痫的危险因素。从长远来看，抑制妊娠期间的醛固酮有不良的营养作用。
The mineralocorticoid aldosterone increases in plasma in healthy pregnancy along with renin and angiotensin II and plays a key role in the physiological plasma volume expansion. In mice, aldosterone contributes to an optimal fetal development by enhancing PlGF (placental growth factor) expression and trophoblast cell proliferation. In preeclampsia, there is coincident suppression of aldosterone and impaired placental development. We hypothesized that aldosterone independently contributes to placental and birth weight in humans, and high dietary sodium and low potassium intakes affect this relationship adversely. We analyzed 24-hour urine collections and plasma samples from gestational week 29 in a subsample of 569 pregnant women from the Odense Child Cohort-a Danish population-based longitudinal cohort study. Plasma and urinary aldosterone were measured by ELISA, sodium and potassium excretions by flame photometer. Predictive values of aldosterone levels and sodium and potassium intakes were assessed by multiple and Cox regression analyses. Primary outcomes were placental weight and birth weight. Secondary outcome was preeclampsia. Urinary aldosterone excretion at gestational week 29 independently contributed to placental and birth weights (adjusted beta-coefficients [95% CI], 24.50 [9.66-39.35] and 9.59 [4.57-14.61], respectively). Aldosterone levels were not associated to preeclampsia incidence. Salt intake >6 g/d was associated with development of preeclampsia (hazard ratio [95% CI], 5.68 [1.51-21.36]). At gestational week 29, urinary aldosterone excretion is an independent predictor of placental and birth weights. High salt intake is a risk factor for preeclampsia. In perspective, suppression of aldosterone in pregnancy has adverse trophic effects.