Tags

Type your tag names separated by a space and hit enter

Fibroblast growth factor 23 and disordered vitamin D metabolism in chronic kidney disease: updating the "trade-off" hypothesis.
Clin J Am Soc Nephrol. 2010 Sep; 5(9):1710-6.CJ

Abstract

The discovery of fibroblast growth factor 23 (FGF23) has clarified much of our understanding of abnormalities in phosphorus and vitamin D metabolism in chronic kidney disease (CKD). FGF23 is a bone-derived hormone that promotes phosphaturia and decreases the synthesis of 1,25-dihydroxyvitamin D (1,25(OH)(2)D). The primary systemic stimuli of FGF23 secretion are increased 1,25(OH)(2)D levels and increased dietary phosphorus intake. In kidney failure, FGF23 levels increase early and steadily rise with progression of kidney disease, likely as an appropriate physiologic adaptation to maintain normal phosphorus balance by helping to augment urinary phosphate excretion in conjunction with increased parathyroid hormone levels and by decreasing gut phosphorus absorption through decreased 1,25(OH)(2)D. In the long term, this compensation may become maladaptive by causing a progressive decline in 1,25(OH)(2)D levels with attendant consequences such as secondary hyperparathyroidism. Moreover, excess FGF23 levels have been independently linked with cardiovascular disease and mortality, suggesting that chronically elevated FGF23 levels may directly contribute to adverse CKD outcomes. Together, these findings have sparked increased interest in elucidating the potential interconnections between dietary phosphorus intake, FGF23, and clinical outcomes in patients with CKD. In addition, given that treatment with activated vitamin D compounds stimulates FGF23, these data have raised important new questions about the optimal use of activated vitamin D compounds in the management of bone and mineral disorders in CKD.

Authors+Show Affiliations

Division of Nephrology and Hypertension, Department of Medicine, University of Miami Miller School of Medicine, Miami, FL 33136, USA. ogutierrez2@med.miami.edu

Pub Type(s)

Journal Article
Research Support, N.I.H., Extramural
Review

Language

eng

PubMed ID

20507957

Citation

Gutiérrez, Orlando M.. "Fibroblast Growth Factor 23 and Disordered Vitamin D Metabolism in Chronic Kidney Disease: Updating the "trade-off" Hypothesis." Clinical Journal of the American Society of Nephrology : CJASN, vol. 5, no. 9, 2010, pp. 1710-6.
Gutiérrez OM. Fibroblast growth factor 23 and disordered vitamin D metabolism in chronic kidney disease: updating the "trade-off" hypothesis. Clin J Am Soc Nephrol. 2010;5(9):1710-6.
Gutiérrez, O. M. (2010). Fibroblast growth factor 23 and disordered vitamin D metabolism in chronic kidney disease: updating the "trade-off" hypothesis. Clinical Journal of the American Society of Nephrology : CJASN, 5(9), 1710-6. https://doi.org/10.2215/CJN.02640310
Gutiérrez OM. Fibroblast Growth Factor 23 and Disordered Vitamin D Metabolism in Chronic Kidney Disease: Updating the "trade-off" Hypothesis. Clin J Am Soc Nephrol. 2010;5(9):1710-6. PubMed PMID: 20507957.
* Article titles in AMA citation format should be in sentence-case
TY - JOUR T1 - Fibroblast growth factor 23 and disordered vitamin D metabolism in chronic kidney disease: updating the "trade-off" hypothesis. A1 - Gutiérrez,Orlando M, Y1 - 2010/05/27/ PY - 2010/5/29/entrez PY - 2010/5/29/pubmed PY - 2011/1/12/medline SP - 1710 EP - 6 JF - Clinical journal of the American Society of Nephrology : CJASN JO - Clin J Am Soc Nephrol VL - 5 IS - 9 N2 - The discovery of fibroblast growth factor 23 (FGF23) has clarified much of our understanding of abnormalities in phosphorus and vitamin D metabolism in chronic kidney disease (CKD). FGF23 is a bone-derived hormone that promotes phosphaturia and decreases the synthesis of 1,25-dihydroxyvitamin D (1,25(OH)(2)D). The primary systemic stimuli of FGF23 secretion are increased 1,25(OH)(2)D levels and increased dietary phosphorus intake. In kidney failure, FGF23 levels increase early and steadily rise with progression of kidney disease, likely as an appropriate physiologic adaptation to maintain normal phosphorus balance by helping to augment urinary phosphate excretion in conjunction with increased parathyroid hormone levels and by decreasing gut phosphorus absorption through decreased 1,25(OH)(2)D. In the long term, this compensation may become maladaptive by causing a progressive decline in 1,25(OH)(2)D levels with attendant consequences such as secondary hyperparathyroidism. Moreover, excess FGF23 levels have been independently linked with cardiovascular disease and mortality, suggesting that chronically elevated FGF23 levels may directly contribute to adverse CKD outcomes. Together, these findings have sparked increased interest in elucidating the potential interconnections between dietary phosphorus intake, FGF23, and clinical outcomes in patients with CKD. In addition, given that treatment with activated vitamin D compounds stimulates FGF23, these data have raised important new questions about the optimal use of activated vitamin D compounds in the management of bone and mineral disorders in CKD. SN - 1555-905X UR - https://www.unboundmedicine.com/medline/citation/20507957/Fibroblast_growth_factor_23_and_disordered_vitamin_D_metabolism_in_chronic_kidney_disease:_updating_the_"trade_off"_hypothesis_ L2 - https://cjasn.asnjournals.org/cgi/pmidlookup?view=long&pmid=20507957 DB - PRIME DP - Unbound Medicine ER -