The association may be explained by multiple mechanisms: (1) iron sequestration and macrophage iron overload promoted by hepcidin, leading to oxidative stress and vascular damage; (2) pro-inflammatory effects, as suggested by correlations with CRP; and (3) an indirect link with anemia management, since patients in higher tertiles were more frequently treated with intravenous iron and ESA therapy. This evidence concerns the gene CRP and anemia (phenotype).