Based on these findings, ADQI proposes that the diagnosis of AKI be reformulated to include not only markers of renal function (e.g., changes in SCr and UO), but also markers of tubular injury such as NGAL, KIM-1, IL-18, and L-FABP (e.g., Figure 1), which, when combined, would not only better characterize the phenotype of AKI and enhance the diagnostic accuracy, but would also detect kidney damage prior to the rise of creatinine, which leads to the identification and treatment of subclinical AKI (Ostermann et al., 2020). This evidence concerns the gene LCN2 and acute kidney injury.