Renal denervation prevents myocardial structural remodeling and arrhythmogenicity in a chronic kidney disease rabbit model

Background: The electrophysiological (EP) effects and safety of renal artery denervation (RDN) in chronic kidney disease (CKD) are unclear. Objective: The purpose of this study was to investigate the arrhythmogenicity of RDN in a rabbit model of CKD. Methods: Eighteen New Zealand white rabbits were randomized to control (n = 6), CKD (n = 6), and CKD-RDN (n = 6) groups. A 5/6 nephrectomy was selected for the CKD model. RDN was applied in the CKD-RDN group. All rabbits underwent cardiac EP studies for evaluation. Immunohistochemistry, myocardial fibrosis, and renal catecholamine levels were evaluated. Results: The CKD group (34.8% ± 9.2%) had a significantly higher ventricular arrhythmia (VA) inducibility than the control (8.6% ± 3.8%; P <.01) and CKD-RDN (19.5% ± 6.3%; P = .01) groups. In the CKD-RDN group, ventricular fibrosis was significantly decreased compared to the CKD group (7.4% ± 2.0 % vs 10.4% ± 3.7%; P = .02). Sympathetic innervation in the CKD group was significantly increased compared to the control and CKD-RDN groups [left ventricle: 4.1 ± 1.8 vs 0.8 ± 0.5 (10² μm²/mm²), P <.01; 4.1 ± 1.8 vs 0.9± 0.6 (10² μm²/mm²), P <.01; right ventricle: 3.6 ± 1.0 vs 1.0 ± 0.4 (10² μm²/mm²), P <.01; 3.6 ± 1.0 vs 1.0 ± 0.5 (10² μm²/mm²), P <.01]. Conclusion: Neuromodulation by RDN demonstrated protective effects with less structural and electrical remodeling, leading to attenuated VAs. In a rabbit model of CKD, RDN plays a therapeutic role by lowering the risk of VA caused by autonomic dysfunction.