Hyperkalemia in chronic kidney disease in the new era of kidney protection therapies.
Abstract
Despite recent therapeutic advances, chronic kidney disease (CKD) is one of the fastest growing global causes of death. This illustrates limitations of current therapeutic approaches and, potentially, unidentified knowledge gaps. For decades, renin-angiotensin-aldosterone system (RAAS) blockers have been the mainstay of therapy for CKD. However, they favor the development of hyperkalemia, which is already common in CKD patients due to the CKD-associated decrease in urinary potassium (K+) excretion and metabolic acidosis. Hyperkalemia may itself be life-threatening as it may trigger potentially lethal arrhythmia, and additionally may limit the prescription of RAAS blockers and lead to low-K+ diets associated to low dietary fiber intake. Indeed, hyperkalemia is associated with adverse kidney, cardiovascular, and survival outcomes. Recently, novel kidney protective therapies, ranging from sodium/glucose cotransporter 2 (SGLT2) inhibitors to new mineralocorticoid receptor antagonists have shown efficacy in clinical trials. Herein, we review K+ pathophysiology and the clinical impact and management of hyperkalemia considering these developments and the availability of the novel K+ binders patiromer and sodium zirconium cyclosilicate, recent results from clinical trials targeting metabolic acidosis (sodium bicarbonate, veverimer), and an increasing understanding of the role of the gut microbiota in health and disease.
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Date
2021-07-27
Type
Corrigendum
Subject
Cardiology, Nephrology/Renal medicine
Collections
Citation
Valdivielso JM, Balafa O, Ekart R, Ferro CJ, Mallamaci F, Mark PB, Rossignol P, Sarafidis P, Del Vecchio L, Ortiz A. Hyperkalemia in Chronic Kidney Disease in the New Era of Kidney Protection Therapies. Drugs. 2021 Sep;81(13):1467-1489. doi: 10.1007/s40265-021-01555-5. Epub 2021 Jul 27. Erratum in: Drugs. 2021 Oct;81(15):1819. doi: 10.1007/s40265-021-01617-8
Journal / Source Title
Drugs
DOI
10.1007/s40265-021-01555-5
PMID
34313978
Publisher
Springer
Publisher’s URL
https://link.springer.com/journal/40265