Associations of dietary phosphorus intake, urinary phosphate excretion, and fibroblast growth factor 23 with vascular stiffness in chronic kidney disease.

Autor:	Houston J; Division of Nephrology and Hypertension, Department of Medicine, University of Miami Miller School of Medicine, Miami, Florida, USA., Smith K, Isakova T, Sowden N, Wolf M, Gutiérrez OM
Jazyk:	angličtina
Zdroj:	Journal of renal nutrition : the official journal of the Council on Renal Nutrition of the National Kidney Foundation [J Ren Nutr] 2013 Jan; Vol. 23 (1), pp. 12-20. Date of Electronic Publication: 2012 Mar 09.
DOI:	10.1053/j.jrn.2011.12.009
Abstrakt:	Objective: Elevated serum phosphate concentrations are established risk factors for cardiovascular disease and mortality in chronic kidney disease (CKD). Independent associations of other indices of phosphorus metabolism, such as phosphorus intake, urinary phosphate excretion, or hormones that regulate these systems, like fibroblast growth factor 23 (FGF23), with markers of cardiovascular disease in CKD, have been studied in less detail. Design: Cross-sectional study. Participants: Seventy-four adult CKD patients with mean creatinine clearance of 51 ± 19 mL/minute. Outcome: Augmentation index (AI)--a surrogate marker of arterial stiffness. Results: Although serum phosphate varied little across quartiles of creatinine clearance, average daily phosphorus intake and 24-hour urinary phosphate excretion decreased from highest to lowest quartile (by 31% and 60%, respectively, P for trend <.05). FGF23 was associated with serum phosphate (r = 0.24, P = .03) and creatinine clearance (r = -0.4, P = .001), but not with dietary phosphorus or 24-hour urinary phosphate excretion (P > .05 for both). Older age, higher systolic blood pressure, female gender, and black race were independently associated with increased AI. In contrast, there were no associations of serum phosphate, dietary phosphorus intake, urinary phosphate excretion, or FGF23 with AI in multivariate-adjusted models. Conclusions: In this sample of patients with CKD, established risk factors for arterial stiffness, but not mediators of phosphorus metabolism, were associated with increased AI. In addition, there were no significant associations between FGF23 and dietary phosphorus or urinary phosphate excretion. Future studies are needed to determine the main factors associated with elevations in FGF23 in CKD and to further assess the association of disordered phosphorus metabolism with subclinical markers of vascular disease. (Copyright © 2013 National Kidney Foundation, Inc. Published by Elsevier Inc. All rights reserved.)
Databáze:	MEDLINE
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