Objectives: Renal sympathetic denervation (RDN) is available and implemented as a strategy for the treatment of resistant hypertension.In the aspect of chronic safety, renal function, as assessed by serum creatinine, eGFR(MDRD), and cystatin C was reported to be unchanged from baseline at 6 months. We investigated whether RDN might cause subtle inflammation and subclinical damage in the early phase of acute kidney injury (AKI). Methods: Female pigs were divided into 6 groups; normal control (group A), Sham-operated control (group B), contrast media control (group C), and renal sympathetic denervation groups subdivided into 3 groups according to the time of sacrifice; immediately (group D), 1 week later (group E), and 2 weeks later (group F) after RDN. We checked IL-1α, 1β, 18, 6, 10, TNF-α, cystatin C, caspase-1, ASC, and NLRP3 as early biomarkers of inflammation and AKI. Results: There were no significant changes in group B and C compared to group A. BUN, serum creatinine, cystatin C, urine protein/creatinine ratio, and urine albumin/creatinine ratio showed a tendency to increase in group D and E and then decrease in group F with no statistical significance. Pro-inflammatory cytokines, IL-1β, 18 increased in group D and E (p<0.05 vs. A), and decreased in group F (p<0.05 vs. D, E) significantly. Casapse-1 activity, ASC, and NLRP3 expressions were also increased in group D (p<0.05 vs. group A), and decreased in group E and F (p<0.05 vs. group D). Conclusion: RDN did not cause clinically significant damages on kidneys. However RDN can induce the activation of pro-inflammatory cytokines, caspase-1 and NLRP3 inflammasome, and then transiently self-limited acute kidney injury.