TY - JOUR
T1 - FGF-23 and the progression of coronary arterial calcification in patients new to dialysis.
AU - Khan, Abigail May
AU - Chirinos, Julio A.
AU - Litt, Harold
AU - Yang, Wei
AU - Rosas, Sylvia E.
N1 - Copyright:
This record is sourced from MEDLINE®/PubMed®, a database of the U.S. National Library of Medicine
PY - 2012/12
Y1 - 2012/12
N2 - Fibroblast growth factor 23 (FGF-23), a regulator of phosphorus metabolism, is a risk marker in CKD. FGF-23 has been associated with coronary arterial calcification (CAC), but it is not known whether FGF-23 predicts CAC progression in CKD. The aim of this study was to evaluate the association of FGF-23 with CAC progression in advanced CKD. FGF-23 levels and CAC were measured by electrocardiography-triggered multislice computed tomography in 99 individuals initiating dialysis. Patients were enrolled in the study from April 2008 to July 2010. CAC was calculated using Agatston and calcium volume score. Sixty-seven study participants had repeat CAC measures at 1 year. Linear regression was used to assess the association of FGF-23 with CAC. The mean age of study participants was 50 years; 33% were women, and 64% were black. The median FGF-23 level was 1238 relative units (RU)/ml (interquartile range, 515-2218 RU/ml). According to Agatston score, FGF-23 was not associated with baseline CAC (P=0.14) but was significantly associated with CAC progression. There was a 192.3-Agatston unit change in CAC score per 1-SD change in FGF-23 (P=0.008) in models adjusting for known risk factors for CAC and serum phosphate. This association persisted after adjustment for high-sensitivity C-reactive protein, 25-OH vitamin D levels, and the use of phosphorus binders. Results were similar when change in calcium volume score was used. In individuals with advanced CKD, serum FGF-23 is strongly associated with CAC progression. FGF-23 may be a marker of cardiovascular risk in CKD.
AB - Fibroblast growth factor 23 (FGF-23), a regulator of phosphorus metabolism, is a risk marker in CKD. FGF-23 has been associated with coronary arterial calcification (CAC), but it is not known whether FGF-23 predicts CAC progression in CKD. The aim of this study was to evaluate the association of FGF-23 with CAC progression in advanced CKD. FGF-23 levels and CAC were measured by electrocardiography-triggered multislice computed tomography in 99 individuals initiating dialysis. Patients were enrolled in the study from April 2008 to July 2010. CAC was calculated using Agatston and calcium volume score. Sixty-seven study participants had repeat CAC measures at 1 year. Linear regression was used to assess the association of FGF-23 with CAC. The mean age of study participants was 50 years; 33% were women, and 64% were black. The median FGF-23 level was 1238 relative units (RU)/ml (interquartile range, 515-2218 RU/ml). According to Agatston score, FGF-23 was not associated with baseline CAC (P=0.14) but was significantly associated with CAC progression. There was a 192.3-Agatston unit change in CAC score per 1-SD change in FGF-23 (P=0.008) in models adjusting for known risk factors for CAC and serum phosphate. This association persisted after adjustment for high-sensitivity C-reactive protein, 25-OH vitamin D levels, and the use of phosphorus binders. Results were similar when change in calcium volume score was used. In individuals with advanced CKD, serum FGF-23 is strongly associated with CAC progression. FGF-23 may be a marker of cardiovascular risk in CKD.
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U2 - 10.2215/CJN.02160212
DO - 10.2215/CJN.02160212
M3 - Article
C2 - 22997345
AN - SCOPUS:84877599062
VL - 7
SP - 2017
EP - 2022
JO - Clinical Journal of the American Society of Nephrology
JF - Clinical Journal of the American Society of Nephrology
SN - 1555-9041
IS - 12
ER -