The Mechanism of Contrast-Induced Acute Kidney Injury and Its Association with Diabetes Mellitus

Figure 2

Cytokines in HGS and CI-AKI. This concentrates mainly on how cytokines are affected by diabetes mellitus (DM)/diabetes nephropathy (DN) or high-glucose status (HGS) and contrast media, which further delineates underlying mechanisms of why DM/DN is a risky factor for contrast-induced kidney injury (CI-AKI). The solid arrows mean increasing, promoting, or activating, and the dotted arrows denote decreasing, weakening, or inactivating. The yellow boxes give the associated cytokines, and most of them increased by DM/DN and then caused apoptosis or necrosis directly or pathologic alteration such as fibrosis and inflammation. TGF-beta and IL-18 cause oxidative stress or apoptosis via some special molecules involved in certain signaling pathways. NOD-like receptor pyrin 3 (NLRP3) is involved in CI-AKI, which is discussed in detail later. Cytokines that relieve renal injury are limited. IL-22 counteracts fibrosis and suppresses NLRP3/caspase-1/IL-1beta. Melatonin alleviates renal damage by reversing IL-33 increase. CTGF, connective tissue growth factor; IFN-γ, interferon-gamma; IL-1/6/18/22/33, interleukin-1/6/18/22/33; MAPK, mitogen-activated protein kinase; Mmp-9, matrix metalloproteinase 9; NLRP3, NOD-like receptor pyrin 3; ROS, reactive oxygen species; TGF-β, tumor growth factor-beta; TNF-α, tumor necrosis factor-alpha.