PTH and acute kidney injury: Several mechanisms may explain increased FGF-23 levels in AKI: (1) increased production by osteocytes and possibly osteoblasts, that escapes regulation by parathyroid hormone, vitamin D signaling, and dietary phosphate restriction [33,34]; (2) increased ectopic production of FGF-23 by damaged renal tubules [33,35]; (3) tubular dysfunction resulting in FGF-23 resistance [36]; (4) and decreased clearance of circulating FGF-23 [14].