Catheter-based renal sympathetic denervation induces acute renal inflammation through activation of caspase-1 and NLRP3 inflammasome

Özet

Objective: Catheter-based renal sympathetic denervation (RDN) is implemented as a strategy to treat resistant hypertension. Serum creatinineand estimated glomerular filtration rate have some limitations to predict the early stage of acute kidney injury (AKI). We investigated the changesof 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 biomarkerswere checked.Results: There were no significant changes in the clinical parameters between the normal control and sham-operated groups using contrastmedia. 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 2after RDN. Caspase-1 increased immediately after RDN until week 2. Apoptosis-associated speck-like protein containing a caspase recruitmentdomain 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. (Anatol J Cardiol2019; 21: 134-41)