Why the study?
Arrhythmias are a major cause of sudden cardiac death in chronic kidney disease, but the molecular mechanisms involved in their development remain poorly understood.
This narrative review highlights the molecular mechanisms of arrhythmias in CKD and discusses the potential of SGLT2 inhibitors as a therapeutic option.
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May guide targeted therapies in CKD arrhythmias; leaves open SGLT2 inhibitor effects on channels without trials.
Chronic kidney disease (CKD) is associated with a significantly increased risk of cardiovascular events and sudden cardiac death. Although arrhythmias are one of the most common causes of sudden cardiac death in CKD patients, the molecular mechanisms involved in the development of arrhythmias are still poorly understood. In this narrative review, therefore, we summarize the current knowledge on the regulation of cardiac ion channels that contribute to arrhythmia in CKD. We do this by first explaining the excitation-contraction coupling, outlining current translational research approaches, then explaining the main characteristics in CKD patients, such as abnormalities in electrolytes and pH, activation of the autonomic nervous system, and the renin-angiotensin-aldosterone system, as well as current evidence for proarrhythmic properties of uremic toxins. Finally, we discuss the substance class of sodium-glucose co-transporter 2 inhibitors (SGLT2i) on their potential to modify cardiac channel regulation in CKD and, therefore, as a treatment option for arrhythmias.
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Sinha et al. (2023) studied this question.
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