Abstract Fibroblast growth factor‐23 ( FGF 23) is a bone‐derived hormone regulating renal phosphate reabsorption and vitamin D synthesis in renal proximal tubules. Here, we show that FGF 23 directly regulates the membrane abundance of the Na + :Cl − co‐transporter NCC in distal renal tubules by a signaling mechanism involving the FGF receptor/αKlotho complex, extracellular signal‐regulated kinase 1/2 ( ERK 1/2), serum/glucocorticoid‐regulated kinase 1 ( SGK 1), and with‐no lysine kinase‐4 ( WNK 4). Renal sodium (Na + ) reabsorption and distal tubular membrane expression of NCC are reduced in mouse models of Fgf23 and α Klotho deficiency. Conversely, gain of FGF 23 function by injection of wild‐type mice with recombinant FGF 23 or by elevated circulating levels of endogenous Fgf23 in Hyp mice increases distal tubular Na + uptake and membrane abundance of NCC , leading to volume expansion, hypertension, and heart hypertrophy in a αKlotho and dietary Na + ‐dependent fashion. The NCC inhibitor chlorothiazide abrogates FGF 23‐induced volume expansion and heart hypertrophy. Our findings suggest that FGF 23 is a key regulator of renal Na + reabsorption and plasma volume, and may explain the association of FGF 23 with cardiovascular risk in chronic kidney disease patients.