To conclude, we showed that increased circulating LCN2 minimally contributes to iron deficiency in CKD, and does not have a determinant role on anemia of CKD, but mediates the stimulatory effects of inflammation on FGF23 production in bone by activating cAMP-mediated signaling, and contributes to the development of cardiac hypertrophy and mortality, likely through stimulation of FGF23 production. This evidence concerns the gene LCN2 and chronic kidney disease.