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

Figure 1

Pathophysiologic changes of CI-AKI in the kidney under HGS. Reactive oxygen species (ROS) are the core factors in both contrast-induced acute kidney injury (CI-AKI) and high-glucose status (HGS). The blue boxes comprise the main procedures of CI-AKI and the yellow ones indicate possible procedures of HGS that strengthen CI-AKI. Hypoxia and ROS production are the common alterations. The arrows link two boxes that show the pathophysiologic direction, which results in final inflammation or cell death. Some additional issues need explanation. Firstly, the vasoactive substances including but not limited to endothelin, adenosine, nitric oxide (NO), and prostaglandin (PG) because all those who are associated with vessel expanding or contracting may affect potential oxygen supply. Secondly, either damaged protein or lipid causes inflammation, apoptosis, or necrosis which are more like damage-associated molecular patterns (DAMPs) discussed later. Thirdly, the CI-AKI mainly results from tubules and endothelia injury.