MIF and acute kidney injury: Our findings can be attributed to the fact that MIF is a proinflammatory cytokine that induces the chemotaxis of macrophages and T cells, evoking an inflammatory response, adding to the fact that it antagonizes the immunosuppressive effect of glucocorticoids—despite being released by glucocorticoids during a stressful kidney event, such as acute kidney injury—thus, it causes an inflammatory process in the kidney leading to activation of macrophages, which subsequently causes the release of more MIF, and a vicious cycle is established [15–17].