IL1B and Sepsis: It is generally believed that the direct trigger of septic AKI is the overwhelming inflammatory response caused by sepsis, which causes the body to produce and release large amounts of cytokines, such as interleukin-1β (IL-1β), interleukin-6 (IL-6), tumor necrosis factor-α (TNF-α), chemokines, and inflammatory mediators, which ultimately lead to renal tubular epithelial cell damage [4].