Associations of Dietary Phosphorus Intake, Urinary Phosphate Excretion, and Fibroblast Growth Factor 23 with Vascular Stiffness in Chronic Kidney Disease

Overview

Journal J Ren Nutr

Specialties Nephrology
Nutritional Sciences

Date 2012 Mar 13

PMID 22406119

Citations 9

Authors

Jessica Houston

Kelsey Smith

Tamara Isakova

Nicole Sowden

Myles Wolf

Orlando M Gutierrez

Affiliations

Soon will be listed here.

Abstract

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.

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