Interestingly, studies involving epidemiological data and animal models [61,62] have demonstrated that the decrease in Klotho expression at the beginning of CKD can lead to the overproduction of FGF-23, which results in secondary hyperparathyroidism, a common complication for patients with CKD [63], which contributes to other important comorbidities detected in this condition, such as CVD. This evidence concerns the gene FGF23 and chronic kidney disease.