Given that CKD and Wnt/β-catenin signaling regulate PRR expression, and FGF23 enhances sodium reabsorption through sodium/chloride cotransporter in the distal tubule [45,46], it can be hypothesized that increased FGF23, Wnt activation, and the downregulation of Klotho in CKD may promote volume overload and an elevation in blood pressure, two well-known risk factors for heart failure. Here, FGF23 is linked to chronic kidney disease.