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Open Access Research article

Fibroblast growth factor 23, mineral metabolism and mortality among elderly men (Swedish MrOs)

Per-Anton Westerberg17*, Åsa Tivesten2, Magnus K Karlsson3, Dan Mellström4, Eric Orwoll5, Claes Ohlsson4, Tobias E Larsson6, Torbjörn Linde1 and Östen Ljunggren1

Author Affiliations

1 Department of Medical Sciences, Uppsala University, Uppsala, Sweden

2 Wallenberg Laboratory for Cardiovascular Research, University of Göteborg, Göteborg, Sweden

3 Clinical and Molecular Osteoporosis Research Unit, Department of Clinical Sciences and Orthopedic Surgery, Lund University, Skåne University Hospital, Lund, Sweden

4 Center for Bone and Arthritis Research at the Sahlgrenska Academy, Institute of Medicine, The Sahlgrenska Academy at Göteborg University, Göteborg, Sweden

5 Oregon Health and Science University, Portland, OR, USA

6 Department of Clinical Science, Intervention and Technology, Karolinska Institute, Stockholm, Sweden

7 Department of Nephrology, Uppsala University, University hospital, Ing 30, 5 tr, Uppsala, SE-751 85, Sweden

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BMC Nephrology 2013, 14:85  doi:10.1186/1471-2369-14-85

Published: 15 April 2013

Abstract

Background

Fibroblast growth factor 23 (FGF23) is the earliest marker of disturbed mineral metabolism as renal function decreases. Its serum levels are associated with mortality in dialysis patients, persons with chronic kidney disease (CKD) and prevalent cardiovascular disease (CVD), and it is associated with atherosclerosis, endothelial dysfunction and left ventricular hypertrophy in the general population. The primary aim of this study is to examine the association between FGF23 and mortality, in relation to renal function in the community. A secondary aim is to examine the association between FGF23 and CVD related death.

Methods

The population-based cohort of MrOS Sweden included 3014 men (age 69–81 years). At inclusion intact FGF23, intact parathyroid hormone (PTH), 25 hydroxyl vitamin D (25D), calcium and phosphate were measured. Mortality data were collected after an average of 4.5 years follow-up. 352 deaths occurred, 132 of CVD. Association between FGF23 and mortality was analyzed in quartiles of FGF23. Kaplan-Meier curves and Log-rank test were used to examine time to events. Cox proportional hazards regression was used to examine the association between FGF23, in quartiles and as a continuous variable, with mortality. The associations were also analyzed in the sub-cohort with estimated glomerular filtration rate (eGFR) above 60 ml/min/1.73 m2.

Results

There was no association between FGF23 and all-cause mortality, Hazard ratio (HR) 95% confidence interval (CI): 1.02 (0.89-1.17). For CVD death the HR (95% CI) was 1.26 (0.99 - 1.59)/(1-SD) increase in log(10)FGF23 after adjustment for eGFR, and other confounders. In the sub-cohort with eGFR > 60 ml/min/1.73 m2 the HR (95% CI) for CVD death was 55% (13–111)/(1-SD) increase in log(10)FGF23.

Conclusions

FGF23 is not associated with mortality of all-cause in elderly community living men, but there is a weak association with CVD death, even after adjustment for eGFR and the other confounders. The association with CVD death is noticeable only in the sub-cohort with preserved renal function.

Keywords:
FGF-23; FGF23; Mineral metabolism; Phosphatonin; Mortality; Elderly