Systemic inflammatory response syndrome (SIRS) characterized by increased levels of circulating cytokines and chemokines, including IL-1β, IL-6, IL-8, MCP-1, and TNF-α, was observed in AKI or ALI patients and animal models, which may cause lung and kidney inflammation, cell apoptosis, increases in endothelial barrier permeability, oxidative stress, and aggravation of pulmonary edema [33,34,41]. This evidence concerns the gene CCL2 and systemic inflammatory response syndrome.