Document Detail


Elevated FGF23 levels are associated with impaired calcium-mediated suppression of PTH in ESRD.
MedLine Citation:
PMID:  20943782     Owner:  NLM     Status:  MEDLINE    
Abstract/OtherAbstract:
CONTEXT: The positive association of elevated fibroblast growth factor-23 (FGF23) with PTH levels in the setting of secondary hyperparathyroidism is paradoxical to the purported effects of FGF23 to suppress PTH secretion.
OBJECTIVE: We used dynamic calcium-mediated suppression of PTH levels in hemodialysis (HD) patients to determine the relationship between FGF23 levels and parathyroid gland function.
DESIGN: HD patients with elevated PTH were washed out of vitamin D analogs and/or calcimimetics and then exposed them to a high-calcium dialysate bath designed to suppress PTH.
SETTING: The study was conducted at an outpatient HD unit of an academic medical center.
PARTICIPANTS: Eighteen maintenance HD patients with elevated PTH levels participated in the study.
MAIN OUTCOME MEASURES: Ionized calcium (iCa), PTH, and FGF23 levels were measured during HD. The slope of the relationship between iCa and PTH (a marker of parathyroid gland mass) and the iCa level required for a 50% reduction in PTH were determined, and the association of these with FGF23 levels was determined.
RESULTS: Increased baseline log FGF23 levels were associated with putative alterations in gland mass as estimated by significantly shallower slopes of the iCa/PTH suppression curves (P = 0.0004), but there was no association between FGF23 and calcium sensing as measured by ionized Ca associated with a 50% suppression of PTH (P = 0.38). FGF23 levels decreased significantly during HD, but this change was not correlated with decrements in either renal phosphate or PTH.
CONCLUSIONS: High FGF23 levels may be a marker for parathyroid gland hyperplasia in HD patients. Acute reductions in neither PTH nor renal phosphate during dialysis correlated with PTH suppression.
Authors:
James B Wetmore; Peter W Santos; Jonathan D Mahnken; Ron Krebill; Rochelle Menard; Hema Gutta; L Darryl Quarles
Publication Detail:
Type:  Journal Article; Research Support, N.I.H., Extramural     Date:  2010-10-13
Journal Detail:
Title:  The Journal of clinical endocrinology and metabolism     Volume:  96     ISSN:  1945-7197     ISO Abbreviation:  J. Clin. Endocrinol. Metab.     Publication Date:  2011 Jan 
Date Detail:
Created Date:  2011-01-06     Completed Date:  2011-02-04     Revised Date:  2013-07-10    
Medline Journal Info:
Nlm Unique ID:  0375362     Medline TA:  J Clin Endocrinol Metab     Country:  United States    
Other Details:
Languages:  eng     Pagination:  E57-64     Citation Subset:  AIM; IM    
Affiliation:
Division of Nephrology and Hypertension, University of Kansas School of Medicine, Kansas City, Kansas 66160, USA. jwetmore@kumc.edu
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MeSH Terms
Descriptor/Qualifier:
Adult
Aged
Calcium / metabolism*,  pharmacology
Female
Fibroblast Growth Factors / blood*
Humans
Hyperparathyroidism, Secondary / blood*,  etiology
Kidney Failure, Chronic / blood*,  complications
Male
Middle Aged
Parathyroid Hormone / blood*
Renal Dialysis
Grant Support
ID/Acronym/Agency:
R01 AR045955/AR/NIAMS NIH HHS; R01AR045955/AR/NIAMS NIH HHS; R56 AR045955/AR/NIAMS NIH HHS; R56AR045955/AR/NIAMS NIH HHS
Chemical
Reg. No./Substance:
0/Parathyroid Hormone; 0/fibroblast growth factor 23; 62031-54-3/Fibroblast Growth Factors; 7440-70-2/Calcium
Comments/Corrections

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