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FGF-23 and vitamin D: don't shoot the messenger?
Author(s) -
Robert Fish,
John Cunningham
Publication year - 2012
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/gfs088
Subject(s) - fibroblast growth factor 23 , medicine , vitamin d and neurology , parathyroid hormone , kidney disease , endocrinology , secondary hyperparathyroidism , fibroblast growth factor , hyperparathyroidism , adverse effect , vitamin , regulator , calcium , biochemistry , receptor , biology , gene
The discovery of fibroblast growth factor-23 (FGF-23) as a key regulator of phosphate and vitamin D metabolism has forced a rethink about the mineral and bone disorder of chronic kidney disease (CKD). FGF-23 powerfully predicts adverse cardiovascular outcomes in patients with CKD and an important question is whether treatment regimens should now be tailored to address FGF-23 levels in addition to those of calcium, phosphate, parathyroid hormone and vitamin D. Nevertheless, despite the known action of active vitamin D therapies to increase FGF-23, this should probably still form an important part of the management of patients with hyperparathyroidism and perhaps at low doses of essentially all patients with advanced renal disease.

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