Inorganic phosphate (Pi) reabsorption in kidneys is required to maintain Pi homeostasis. Renal Pi transport is mediated by the sodium-dependent phosphate transporters, NaPi-IIa, NaPi-IIc, and Pit2 in the brush border membrane of the proximal tubule (BBM). Dietary Pi intake regulates these transporters. We investigated in WT and NaPi-IIa KO mice the chronic and acute adaption to dietary Pi. Mice received 5 days a 1.2% (HPD) or 0.1% Pi diet (LPD). On day 5, some mice were switched for 4 hours to LPD or HPD. Serum Pi was similar under chronic diets in WT and KO, but KO mice reduced their serum Pi when acutely switched to LPD. Urinary Pi excretion was similar in WT and KO mice under HPD, but under a chronic LPD KO mice exhibited a constant urinary Pi loss compensated by a higher intestinal Pi absorption. During the acute HPD-to-LPD switch, KO mice exhibited a delayed decrease in urinary Pi excretion. In WT mice PTH was acutely regulated by Pi diet, whereas FGF23 level exhibited a slower response in the acute HPD-to-LPD. In BBM vesicles, Pi transport activity and plasma membrane NaPi-IIa but not NaPi-IIc or Pit2 abundance acutely adapted to diets in WT mice. In KO BBM vesicles transport activity was lower under each conditions and did not adapt.Thus, NaPi-IIa mediates the fast adaptation to Pi intake and is upregulated during the adaptation to low Pi despite high FGF23 levels.