Therefore, we designed a before�Cafter study to reduce the effect of individual differences, because large animals can be conveniently and repeatedly monitored. In Fukunaga et al��s study, no significant differences were observed in the effective refractory period of the left atrium between the sham and model groups. The effective refractory period of the right atrium also showed no significant difference between the sham and model groups in our study, whereas a significant difference was observed between baseline and 2 weeks in the model group. Overactivity of the SNS might play an important role in shortening of the effective refractory period because just adrenergic stimulation can decrease the human AERP by approximately 5%. Our model was suitable for further determining the predominant factors that enhance AF vulnerability. Predicted mechanisms for the development of AF associated with CKD were observed in our study, including RAAS, SNS activation and atrial fibrosis. There was also a trend for an Lincomycin hydrate increase in plasma hs-CRP levels in the model group, but this was not significant. CRP, as a marker of inflammation, is elevated in chronic renal impairment. Serum CRP concentrations are positively correlated with AF persistence, and predict postoperative AF occurrence. The RAAS is activated by renal ischemic impairment and increased sympathetic activation in CKD. The RAAS is involved in the pathogenesis of interstitial fibrosis, and they create a substrate for AF. The injured kidney��s Lipoamide afferent signals to central integrative structures in the brain lead to increased sympathetic activation. Chemoreflex activation, reduced nitric oxide availability, and renalase secretion are also involved in heightened sympathetic tone and increased noradrenaline levels in patients with kidney impairment. Increased sympathetic activation is found in the initial clinical stages of CKD, which also leads to atrial remodeling processes, possibly by neurohumoral activation and changes in atrial hemodynamics. Hyper-sympathetic activity may facilitate the initiation of AF and acute atrial electrophysiological changes.