Apart from the phenotypic differences in adulthood vs. childhood concerning FGF23 and phosphate metabolism, these anomalies seem to be ADPDK specific, as markedly FGF23 elevation is only found in non-ADPKD patients with advanced CKD stage, where it is thought to counteract phosphate retention and is classically accompanied by an increased parathyroid hormone and decreased 1,25-dihydroxyvitamin D levels (14). This evidence concerns the gene FGF23 and autosomal dominant polycystic kidney disease.