In addition to these changes related to PTC injury, our experimental model (Figure 1) also reproduced the pro-inflammatory activation of PTCs that contributes to leukocyte-mediated renal injury in AKI [4]: under hypoxic/hyperglycemic/inflammatory conditions, there was an increase in HK-2 cells in the secretion of the chemokines IL-8 and MCP-1 and the expression of the leukocyte adhesion molecule ICAM-1 (Figure 1). This evidence concerns the gene CCL2 and acute kidney injury.