, Jeong-Su Kim 2
, Il Young Kim 1
, Hyang Sook Kim 3
, Joo-Young Kim 3
, Harin Rhee 1
, Eun Young Seong 1
, Sang Heon Song 1
, Soo Bong Lee 1
, Charles Louis Edelstein 4
, Ihm Soo Kwak 1
2Division of Cardiology, Department of Internal Medicine, School of Medicine, Pusan National University; Busan-Republic of Korea
3Research Institute for Convergence of Biomedical Science and Technology, Pusan National University, Yangsan Hospital; Yangsan-Republic of Korea
4Division of Renal Diseases and Hypertension, University of Colorado Denver; Aurora, Colorado-USA
Abstract
Objective: Catheter-based renal sympathetic denervation (RDN) is implemented as a strategy to treat resistant hypertension. Serum creatinine and estimated glomerular filtration rate have some limitations to predict the early stage of acute kidney injury (AKI). We investigated the changes of early inflammatory biomarkers in AKI following the RDN procedure.
Methods: Twenty-five female swine were divided into three groups: normal control (Normal, n=5), sham-operated (Sham, n=5), and RDN groups (RDN, n=15). The RDN group was further subdivided into three subgroups according to the time of sacrifice: immediately (RDN-0, n=5), 1 week (RDN-1, n=5), and 2 weeks (RDN-2, n=5) after RDN. Renal cortical tissue was harvested, and clinical parameters and inflammatory biomarkers were checked.
Results: There were no significant changes in the clinical parameters between the normal control and sham-operated groups using contrast media. Inflammatory interleukin (IL)-1β, IL-18, IL-6, tumor necrosis factor-α, and anti-inflammatory IL-10 increased immediately and then decreased at week 2 after RDN in the renal cortical tissue. Leaderless protein, IL-1α level, increased at week 1 and then decreased at week 2 after RDN. Caspase-1 increased immediately after RDN until week 2. Apoptosis-associated speck-like protein containing a caspase recruitment domain and NLRP3 expressions increased immediately and then decreased at week 2 after RDN.
Conclusion: The RDN could induce acute renal inflammation through the activation of caspase-1 and NLRP3 inflammasome.