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NDT Advance Access originally published online on March 22, 2006
Nephrology Dialysis Transplantation 2006 21(7):1984-1987; doi:10.1093/ndt/gfl106
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© The Author [2006]. Published by Oxford University Press on behalf of ERA-EDTA. All rights reserved. For Permissions, please email: journals.permissions@oxfordjournals.org

Case Report

Blood pressure reduction in pregnancy by sodium chloride

Stefan Farese, Kushiar Shojaati, Bert Kadereit, Felix J. Frey and Markus G. Mohaupt

Department of Nephrology and Hypertension, University of Berne, Inselspital, CH-3010 Berne, Switzerland

Correspondence and offprint requests to: Markus G. Mohaupt, University Hospital Berne, Department of Nephrology/Hypertension, 3010 Berne, Switzerland. Email: markus.mohaupt@insel.ch

Keywords: aldosterone; arterial hypertension; hypoaldosteronism; pregnancy; sodium chloride

The first 10% of the full text of this article appears below.

Volume expansion in the presence of elevated aldosterone availability is a hallmark of normal pregnancy. Intravascular volume depletion characterizes severe pregnancy-associated disease conditions such as intra-uterine growth retardation, chronic hypertension or pre-eclampsia [1]. Two hypotheses have been forwarded to explain volume depletion in pregnancy: the first hypothesis charges inappropriate sensing of vascular ‘overfilling’, resulting in an increased transendothelial loss of fluid to the extravascular compartment. In contrast, the second hypothesis focuses on vascular ‘underfilling’ due to inappropriately low aldosterone levels. The second hypothesis is based on the assumption that a compensatory increase in the circulating fluid volume is required in normal pregnancy to support fetal substrate delivery. According to the second concept, maternal blood pressure increases due to counter-regulatory mechanisms when placental blood supply is reduced [2]. In support of the ‘underfilling’ hypothesis are observations that a . . . [Full Text of this Article]



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