Mineral (Mal)Adaptation to Kidney Disease—Young Investigator Award Address
Author(s) -
Myles Wolf
Publication year - 2015
Publication title -
clinical journal of the american society of nephrology
Language(s) - Uncategorized
Resource type - Journals
SCImago Journal Rank - 2.755
H-Index - 151
eISSN - 1555-905X
pISSN - 1555-9041
DOI - 10.2215/cjn.04430415
Subject(s) - fibroblast growth factor 23 , medicine , biomarker , kidney disease , fibroblast growth factor , bone mineral , disease , regulator , bioinformatics , endocrinology , intensive care medicine , physiology , parathyroid hormone , osteoporosis , calcium , receptor , biology , biochemistry , gene
In the short time since its initial discovery as the cause of rare hypophosphatemic disorders, fibroblast growth factor-23 (FGF-23) has emerged as a major regulator of mineral metabolism and critical component of the bone and mineral adaptation to CKD. However, because elevated FGF-23 levels are also a novel biomarker and possible molecular mediator of increased risks of cardiovascular disease and death in CKD, the initially adaptive response to increase FGF-23 levels to maintain neutral phosphate balance in CKD may ultimately become maladaptive. Incorporating FGF-23 into understanding the complex physiology that governs normal bone and mineral metabolism and its alterations in CKD has filled critical knowledge gaps and opened a new landscape of exciting hypotheses and novel therapeutic strategies to be tested in the continued quest to alleviate the burden of CKD.
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