Randomized Controlled Trial
Copyright ©The Author(s) 2015. Published by Baishideng Publishing Group Inc. All rights reserved.
World J Nephrol. Jul 6, 2015; 4(3): 423-437
Published online Jul 6, 2015. doi: 10.5527/wjn.v4.i3.423
Changes in urinary excretion of water and sodium transporters during amiloride and bendroflumethiazide treatment
Janni M Jensen, Frank H Mose, Anna-Ewa O Kulik, Jesper N Bech, Robert A Fenton, Erling B Pedersen
Janni M Jensen, Frank H Mose, Anna-Ewa O Kulik, Jesper N Bech, Erling B Pedersen, University Clinic in Nephrology and Hypertension, Department of Medical Research, Holstebro Hospital, Regional Hospital Jutland West and Aarhus University, 7500 Holstebro, Denmark
Robert A Fenton, Department of Biomedicine, Aarhus University, 8000 Aarhus, Denmark
Author contributions: All authors had contributed to the manuscript; Jensen JM, Mose FH and Pedersen EB designed the project; Jensen JM, Mose FH and Kulik AEO performed the experiments and statistical analyzes; Fenton RA performed the NKCC2 antibody characterization; Jensen JM, Mose FH, Bech JN, Fenton RA and Pedersen EB wrote and edited the manuscript; all authors read and approved the final manuscript.
Supported by Grants from The Lundbeck Foundation, Aase and Ejnar Danielsens Foundation, Helen and Ejnar Bjoernows Foundation and Region Midjutlands Research Fund.
Ethics approval statement: This study was review and approved by the Regional Committees on Health Research Ethics, Skottenborg 26, 8600 Viborg, Denmark (j.no 1-10-72-178-12).
Clinical trial registration: This study is registered at clinical trials. The registration identification number is: NCT 01635231 http://clinicaltrials.gov/ct2/show/NCT01635231.
Informed consent statement: All study participants provided informed written consent prior to study enrolment.
Conflict-of-interest statement: The authors declare that they have no competing interests.
Data sharing statement: No additional data are available.
Open-Access: This article is an open-access article which was selected by an in-house editor and fully peer-reviewed by external reviewers. It is distributed in accordance with the Creative Commons Attribution Non Commercial (CC BY-NC 4.0) license, which permits others to distribute, remix, adapt, build upon this work non-commercially, and license their derivative works on different terms, provided the original work is properly cited and the use is non-commercial. See: http://creativecommons.org/licenses/by-nc/4.0/
Correspondence to: Janni M Jensen, PhD, University Clinic in Nephrology and Hypertension, Department of Medical Research, Holstebro Hospital, Regional Hospital Jutland West and Aarhus University, Laegaardvej 12, 7500 Holstebro, Denmark. jannimaj@gmail.com
Telephone: +45-7843-6588 Fax: +45-7843-6582
Received: November 13, 2014
Peer-review started: November 18, 2014
First decision: February 7, 2015
Revised: March 8, 2015
Accepted: April 28, 2015
Article in press: April 30, 2015
Published online: July 6, 2015
Core Tip

Core tip: Measurements of urinary sodium-potassium chloride co-transporter (NKCC2), epithelial sodium channel (ENaC) and aquaporin2 (AQP2) can be used as biomarkers of water- and sodium transport in the nephron. However, it has never been studied to what extent the function of NKCC2, ENaC and AQP2 is simultaneously affected in response to diuretics. The present study showed that infusion of 3% saline increased u-NKCC2 and u-AQP2 during amiloride and placebo, while u-NKCC2 and u-AQP2 remained unchanged during bendroflumethiazide. Therefor, in contrast to amiloride, bendroflumethiazide caused the absence of a compensatory reabsorption of sodium via NKCC2 and water via AQP2.