The role of cardiovascular diseases as predictors of ESA hyporesponsiveness has been previously studied [18, 29] in CKD patients and the most liable mechanism is related to an increased production of inflammatory cytokines, such as interleukins 1 and 6, Tumor Necrosis Factor and interferon, which induce apoptosis in erythroid progenitor cells and decrease the iron availability by stimulating hepcidin production [30]. This evidence concerns the gene HAMP and chronic kidney disease.