There were distinct pathophysiological changes in sepsis-induced AKI compared to non sepsis-induced AKI reflected by special biomarkers, including interleukin-18 (IL-18) whose concentrations were higher in urine of sepsis induced AKI patients [5] Various serum and urinary biomarkers have been found to be up-regulated in kidney injury, such as liver fatty-acid binding protein, cystatin C, kidney injury molecule-1 and neutrophil gelatinase-associated lipocalin [6]. This evidence concerns the gene CST3 and acute kidney injury.