Aldosterone, Salt, and Potassium Intakes as Predictors of Pregnancy Outcome, Including Preeclampsia

Anna Birukov, Louise Bjørkholt Andersen, Florian Herse, Natalia Rakova, Gitte Kitlen, Henriette Boye Kyhl, Michaela Golic, Nadine Haase, Kristin Kräker, Dominik N Müller, Jan Stener Jørgensen, Marianne Skovsager Andersen, Ralf Dechend, Boye L Jensen*

*Corresponding author for this work

Research output: Contribution to journalJournal articleResearchpeer-review

Abstract

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 β-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.

Original languageEnglish
JournalHypertension
Volume74
Issue number2
Pages (from-to)391-398
ISSN0194-911X
DOIs
Publication statusPublished - Aug 2019

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Pre-Eclampsia
Aldosterone
Potassium
Salts
Placentation
Mineralocorticoids
Urine Specimen Collection
Plasma Volume
Trophoblasts
Renin
Longitudinal Studies
Pregnant Women
Cohort Studies
Regression Analysis
Cell Proliferation
Weights and Measures
Incidence

Cite this

@article{b096e24531134ae0911b5c36fd56e9d5,
title = "Aldosterone, Salt, and Potassium Intakes as Predictors of Pregnancy Outcome, Including Preeclampsia",
abstract = "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 β-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.",
author = "Anna Birukov and Andersen, {Louise Bj{\o}rkholt} and Florian Herse and Natalia Rakova and Gitte Kitlen and Kyhl, {Henriette Boye} and Michaela Golic and Nadine Haase and Kristin Kr{\"a}ker and M{\"u}ller, {Dominik N} and J{\o}rgensen, {Jan Stener} and Andersen, {Marianne Skovsager} and Ralf Dechend and Jensen, {Boye L}",
year = "2019",
month = "8",
doi = "10.1161/HYPERTENSIONAHA.119.12924",
language = "English",
volume = "74",
pages = "391--398",
journal = "Hypertension",
issn = "0194-911X",
publisher = "Lippincott Williams & Wilkins",
number = "2",

}

Aldosterone, Salt, and Potassium Intakes as Predictors of Pregnancy Outcome, Including Preeclampsia. / Birukov, Anna; Andersen, Louise Bjørkholt; Herse, Florian; Rakova, Natalia; Kitlen, Gitte; Kyhl, Henriette Boye; Golic, Michaela; Haase, Nadine; Kräker, Kristin; Müller, Dominik N; Jørgensen, Jan Stener; Andersen, Marianne Skovsager; Dechend, Ralf; Jensen, Boye L.

In: Hypertension, Vol. 74, No. 2, 08.2019, p. 391-398.

Research output: Contribution to journalJournal articleResearchpeer-review

TY - JOUR

T1 - Aldosterone, Salt, and Potassium Intakes as Predictors of Pregnancy Outcome, Including Preeclampsia

AU - Birukov, Anna

AU - Andersen, Louise Bjørkholt

AU - Herse, Florian

AU - Rakova, Natalia

AU - Kitlen, Gitte

AU - Kyhl, Henriette Boye

AU - Golic, Michaela

AU - Haase, Nadine

AU - Kräker, Kristin

AU - Müller, Dominik N

AU - Jørgensen, Jan Stener

AU - Andersen, Marianne Skovsager

AU - Dechend, Ralf

AU - Jensen, Boye L

PY - 2019/8

Y1 - 2019/8

N2 - 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 β-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.

AB - 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 β-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.

U2 - 10.1161/HYPERTENSIONAHA.119.12924

DO - 10.1161/HYPERTENSIONAHA.119.12924

M3 - Journal article

VL - 74

SP - 391

EP - 398

JO - Hypertension

JF - Hypertension

SN - 0194-911X

IS - 2

ER -