Proteinuria and protein overload to the tubular system, which develops in several forms of chronic kidney diseases, is considered to be a key factor that triggers the activation of proximal tubular epithelial cells to produce and/or secrete into the interstitium various inflammatory mediators, including interleukin (IL)-6, IL-8, monocyte chemoattractant peptide 1 (MCP-1/CCL2), RANTES/CCL5, and the intercellular adhesion molecule 1, but also fibrotic molecules such as connective tissue growth factor (CTGF) and fibronectin [21]. This evidence concerns the gene CCL5 and chronic kidney disease.