FGF23 and acute kidney injury: Mechanistically, several factors are involved in AKI-induced cardiac dysfunction including increased volume overload, acid-base and hydroelectrolyte imbalance, activation of the renin–angiotensin–aldosterone system (RAAS), and accumulation of uremic toxins such as indoxyl sulfate or fibroblast growth factor 23 (FGF-23), which can cause direct myocardial damage [131,132,133].