IL1B and Sepsis: Sepsis-induced overwhelming inflammatory response results in the production and release of a large amount of cytokines such as tumor necrosis factor-α (TNF-α), interleukin-1β (IL-1β), interleukin-6 (IL-6), inflammatory mediators and chemokines, which is considered as the direct trigger of septic AKI and eventually lead to renal tubular epithelial cell injury [5].