Elevated FGF-23 in a patient with rhabdomyolysis-induced acute kidney injury | Zendy

David E. Leaf | Zendy; Myles Wolf | Zendy; Leonard Stern | Zendy

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Elevated FGF-23 in a patient with rhabdomyolysis-induced acute kidney injury

Author(s) -

David E. Leaf,

Myles Wolf,

Leonard Stern

Publication year - 2009

Publication title -

nephrology dialysis transplantation

Language(s) - English

Resource type - Journals

SCImago Journal Rank - 1.654

H-Index - 168

eISSN - 1460-2385

pISSN - 0931-0509

DOI - 10.1093/ndt/gfp682

Subject(s) - medicine , rhabdomyolysis , hypocalcaemia , fibroblast growth factor 23 , acute kidney injury , parathyroid hormone , endocrinology , vitamin d deficiency , gastroenterology , vitamin d and neurology , calcium

Rhabdomyolysis-induced acute kidney injury (AKI) is characterized by hyperphosphataemia and hypocalcaemia. Despite appropriate secondary elevation of parathyroid hormone (PTH) in response to hypocalcaemia, rhabdomyolysis and AKI are associated with acute deficiency of 1,25-dihydroxycholecalciferol (1,25(OH)(2)D(3)), and yet, the mechanism responsible for such a deficiency remains unclear. Fibroblast growth factor 23 (FGF-23), a potent phosphaturic hormone that inhibits 25-hydroxyvitamin D(3)-1alpha-hydroxylase, could explain the deficiency of 1,25(OH)(2)D(3) in this setting. Here, we document, for the first time, elevated levels of FGF-23 in a patient with rhabdomyolysis-induced AKI.

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