Activation of the renin–angiotensin–aldosterone system, hyperuricaemia, uraemic toxins such as asymmetric dimethylarginine, hyperphosphataemia, abnormal bone mineral metabolism, elevated levels of hormones that regulate phosphate (parathyroid hormone and fibroblast growth factor-23 (FGF-23)), oxidative stress and chronic low-grade inflammation have all been implicated in the development of myocardial hypertrophy, fibrosis and increased cardiovascular mortality.2 This evidence concerns the gene FGF23 and cardiac hypertrophy.