These results together with the absence of cardiac hypertrophy in the CKD mouse model indicate that the alterations in cardiac repolarization are associated to the high FGF23 and low Klotho levels present in uremia in the absence of relevant structural cardiac remodeling, although it is important to note that our CKD model presents with other uremia-associated alterations, and, therefore, it is not possible to claim that FGF23 is the sole responsible factor for the increased QT interval in the context of CKD. This evidence concerns the gene FGF23 and cardiac hypertrophy.