A persistent inflammation induced by high-glucose is a leading cause of DKD via the activation of the generated advanced glycation end product (AGE) pathway, protein kinase C pathway, and polyol pathway, which promotes the expression of cytokines (such as monocyte-chemotactic protein-1, interleukin-1β, and toll-like receptors (TLRs) related to inflammatory pathways and macrophage infiltration leading to insulin resistance, proteinuria, and renal interstitial fibrosis (18–20). This evidence concerns the gene CCL2 and diabetic kidney disease.