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©The Author(s) 2017. Published by Baishideng Publishing Group Inc. All rights reserved.
Application of established pathophysiologic processes brings greater clarity to diagnosis and treatment of hyponatremia
John K Maesaka, Louis J Imbriano, Nobuyuki Miyawaki, Department of Medicine and Division of Nephrology and Hypertension, Winthrop-University Hospital, Mineola, NY 11501, United States
Author contributions: All the authors contributed to this manuscript.
Conflict-of-interest statement: No conflict of interest.
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: John K Maesaka, MD, Department of Medicine and Division of Nephrology and Hypertension, Winthrop-University Hospital, 200 Old Country Road, Suite 135, Mineola, NY 11501, United States. jmaesaka@winthrop.org
Telephone: +1-516-6632169 Fax: +1-516-6632179
Received: September 20, 2016
Peer-review started: September 24, 2016
First decision: October 20, 2016
Revised: December 6, 2016
Accepted: December 27, 2016
Article in press: December 28, 2016
Published online: March 6, 2017
Processing time: 166 Days and 1.6 Hours
Peer-review started: September 24, 2016
First decision: October 20, 2016
Revised: December 6, 2016
Accepted: December 27, 2016
Article in press: December 28, 2016
Published online: March 6, 2017
Processing time: 166 Days and 1.6 Hours
Core Tip
Core tip: When dealing with normo-volemic, non-edematous hyponatremic patients the initial treatment should be i.v. normal saline, combined with measuring the fractional excretion of urate. As serum sodium is corrected, the patients with syndrome of inappropriate antidiuresis (SIAD) will normalize the fractional excretion of urate, while patients with cerebral-renal salt wasting will have a persistently elevated fractional excretion of urate. It appears that patients with SIAD will have a slow or no increase in serum sodium with saline, while patients with renal salt wasting will have a more rapid increase in serum sodium.