Key result
Uremic toxins, particularly indoxyl sulfate, promote the development and progression of atrial fibrillation through mechanisms involving myocardial fibrosis, inflammation, and oxidative stress.
Why the study?
CKD and AF are closely associated, with recent attention focusing on the role of uremic toxins such as indoxyl sulfate in AF pathogenesis.
This review highlights the mechanistic role of uremic toxins like indoxyl sulfate in promoting atrial fibrillation, suggesting they may serve as both predictors of recurrence and potential therapeutic targets in patients with chronic kidney disease.
Atrial fibrillation (AF) is the most prevalent arrhythmia in the general population. There is a close association between chronic kidney disease (CKD) and AF. In recent years, attention has been focused on the relationship between AF and uremic toxins, including indoxyl sulfate (IS). Several animal studies have shown that IS promotes the development and progression of AF. IS has been shown to cause fibrosis and inflammation in the myocardium and exacerbate AF by causing oxidative stress and reducing antioxidative defense. Administration of AST-120, an absorbent of uremic toxins, decreases uremic toxin-induced AF in rodents. We have recently reported that patients with a higher serum IS level exhibit a higher rate of AF recurrence after catheter ablation, with serum IS being a significant predictor of AF recurrence. In this review, we discuss the possible mechanisms behind the AF-promoting effects of uremic toxins and summarize the reported clinical studies of uremic toxin-induced AF.
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Yamagami et al. (2019) conducted a review in Atrial fibrillation and chronic kidney disease. Uremic toxins (indoxyl sulfate) was evaluated. Uremic toxins, particularly indoxyl sulfate, promote the development and progression of atrial fibrillation through mechanisms involving myocardial fibrosis, inflammation, and oxidative stress.
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