Moreover, various immunological alterations (e.g., infiltration of immune cells into the kidney and release of proinflammatory factors and upregulation of cytokines such as IL-1 (interleukin-1), IL-18, IL-6, IL-33, TGF-β (tumor growth factor-beta), IFN-c (interferon-gamma), and TNF-α (tumor necrosis factor-alpha)) among patients with DM, could directly or indirectly facilitate AKI (particularly CI-AKI) [23]. This evidence concerns the gene IL33 and diabetes mellitus.