Editorial
Copyright ©The Author(s) 2017. Published by Baishideng Publishing Group Inc. All rights reserved.
World J Nephrol. Mar 6, 2017; 6(2): 59-71
Published online Mar 6, 2017. doi: 10.5527/wjn.v6.i2.59
Application of established pathophysiologic processes brings greater clarity to diagnosis and treatment of hyponatremia
John K Maesaka, Louis J Imbriano, Nobuyuki Miyawaki
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
Abstract

Hyponatremia, serum sodium < 135 mEq/L, is the most common electrolyte abnormality and is in a state of flux. Hyponatremic patients are symptomatic and should be treated but our inability to consistently determine the causes of hyponatremia has hampered the delivery of appropriate therapy. This is especially applicable to differentiating syndrome of inappropriate antidiuresis (SIAD) from cerebral salt wasting (CSW) or more appropriately, renal salt wasting (RSW), because of divergent therapeutic goals, to water-restrict in SIAD and administer salt and water in RSW. Differentiating SIAD from RSW is extremely difficult because of identical clinical parameters that define both syndromes and the mindset that CSW occurs rarely. It is thus insufficient to make the diagnosis of SIAD simply because it meets the defined characteristics. We review the pathophysiology of SIAD and RSW, the evolution of an algorithm that is based on determinations of fractional excretion of urate and distinctive responses to saline infusions to differentiate SIAD from RSW. This algorithm also simplifies the diagnosis of hyponatremic patients due to Addison’s disease, reset osmostat and prerenal states. It is a common perception that we cannot accurately assess the volume status of a patient by clinical criteria. Our algorithm eliminates the need to determine the volume status with the realization that too many factors affect plasma renin, aldosterone, atrial/brain natriuretic peptide or urine sodium concentration to be useful. Reports and increasing recognition of RSW occurring in patients without evidence of cerebral disease should thus elicit the need to consider RSW in a broader group of patients and to question any diagnosis of SIAD. Based on the accumulation of supporting data, we make the clinically important proposal to change CSW to RSW, to eliminate reset osmostat as type C SIAD and stress the need for a new definition of SIAD.

Keywords: Hyponatremia; Cerebral-renal salt wasting; Fractional excretion of urate

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.