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Updated: Nov 5, 2025
Improved Renal Denervation Mitigated Hypertension Induced by Angiotensin II Infusion
Published on: May 26, 2022
Renal denervation prevents myocardial structural remodeling and arrhythmogenicity in a chronic kidney disease rabbit
Shin-Huei Liu1, Li-Wei Lo1, Yu-Hui Chou1
1Division of Cardiology, Department of Medicine, Taipei Veterans General Hospital, Taipei, Taiwan; Institute of Clinical Medicine and Cardiovascular Research Institute, National Yang Ming Chiao Tung University, Taipei, Taiwan.
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.
Insights
Renal artery denervation (RDN) reduced ventricular arrhythmias in a chronic kidney disease (CKD) rabbit model. RDN offers a therapeutic role by mitigating autonomic dysfunction and lowering VA risk in CKD patients.
Area of Science:
- Cardiovascular Research
- Nephrology
- Electrophysiology
Background:
- Electrophysiological effects and safety of renal artery denervation (RDN) in chronic kidney disease (CKD) remain largely uncharacterized.
- Autonomic dysfunction in CKD is linked to increased cardiovascular complications, including arrhythmias.
Purpose of the Study:
- To investigate the arrhythmogenic potential of RDN in a rabbit model of CKD.
- To evaluate the impact of RDN on cardiac electrophysiology and structural remodeling in CKD.
Main Methods:
- A 5/6 nephrectomy model was used to induce CKD in New Zealand white rabbits.
- Rabbits were randomized into control, CKD, and CKD with RDN groups.
- Cardiac electrophysiological studies, immunohistochemistry, fibrosis assessment, and catecholamine level analysis were performed.
Main Results:
- CKD significantly increased ventricular arrhythmia (VA) inducibility compared to controls.
- RDN in CKD rabbits significantly reduced VA inducibility compared to the CKD-only group.
- RDN attenuated ventricular fibrosis and normalized sympathetic innervation in CKD rabbits.
Conclusions:
- Neuromodulation via RDN demonstrates protective effects against structural and electrical remodeling in CKD.
- RDN plays a therapeutic role in reducing the risk of VA associated with autonomic dysfunction in CKD.
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