Serum potassium changes during hypothermia and rewarming: a case series and hypothesis on the mechanism.

Autor: Boubes K; Northwestern University Feinberg School of Medicine, Chicago, IL, USA.; Ohio State University, Columbus, OH, USA., Batlle D; Northwestern University Feinberg School of Medicine, Chicago, IL, USA., Tang T; Northwestern University Feinberg School of Medicine, Chicago, IL, USA.; Foothills Nephrology, Spartanburg, SC, USA., Torres J; Northwestern University Feinberg School of Medicine, Chicago, IL, USA., Paul V; Northwestern University Feinberg School of Medicine, Chicago, IL, USA., Abdul HM; Northwestern University Feinberg School of Medicine, Chicago, IL, USA., Rosa RM; Northwestern University Feinberg School of Medicine, Chicago, IL, USA.
Jazyk: angličtina
Zdroj: Clinical kidney journal [Clin Kidney J] 2022 Jun 22; Vol. 16 (5), pp. 827-834. Date of Electronic Publication: 2022 Jun 22 (Print Publication: 2023).
DOI: 10.1093/ckj/sfac158
Abstrakt: Introduction: Hypokalemia is known to occur in association with therapeutically induced hypothermia and is usually managed by the administration of potassium (K + ).
Methods: We reviewed data from 74 patients who underwent a therapeutic hypothermia protocol at our medical institution.
Results: In four patients in whom data on serum K + and temperature were available, a strong positive correlation between serum K + and body temperature was found. Based on the close positive relationship between serum K + and total body temperature, we hypothesize that serum K + decreases during hypothermia owing to decreased activity of temperature-dependent K + exit channels that under normal conditions are sufficiently active to match cellular K + intake via sodium/K + /adenosine triphosphatase. Upon rewarming, reactivation of these channels results in a rapid increase in serum K + as a result of K + exit down its concentration gradient.
Conclusion: Administration of K + during hypothermia should be done cautiously and avoided during rewarming to avoid potentially life-threatening hyperkalemia. K + exit via temperature-dependent K + channels provides a logical explanation for the rebound hyperkalemia. K + exit channels may play a bigger role than previously appreciated in the regulation of serum K + during normal and pathophysiological conditions.
Competing Interests: The results presented in this article have not been published previously in part or in whole, except in abstract format. D.B. is coinventor of patents entitled ‘Active low molecular weight variants of angiotensin converting enzyme 2 (ACE2)’, ‘Active low molecular weight variants of angiotensin converting enzyme 2 (ACE2) for the treatment of diseases and conditions of the eye’ and ‘Soluble ACE2 variants and uses therefor’; is founder of Angiotensin Therapeutics Inc.; has received consulting fees from AstraZeneca, Relypsa and Tricida, all unrelated to this work and received unrelated support from the National Institute of Diabetes and Digestive and Kidney Diseases (grant R01DK104785) as well as from a grant from AstraZeneca. All remaining authors have nothing to disclose related to this publication.
(© The Author(s) 2022. Published by Oxford University Press on behalf of the ERA.)
Databáze: MEDLINE
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