These in vitro findings are supported by data originating from various rodent models with elevated serum FGF23 levels, such as administration of recombinant FGF23 in wild-type mice, renal ablation in rats, αKlotho hypomorphic mice and administration of high phosphate or adenine diets in mice, which display adverse outcomes that are associated with CKD such as renal fibrosis, systemic inflammation, anemia and cardiac hypertrophy [90,92,98,100,101,102,103]. This evidence concerns the gene FGF23 and chronic kidney disease.