Abstract
BackgroundFibroblast growth factor23 (FGF23) is elevated in CKD and has been associated with outcomes such as death, cardiovascular (CV) events and progression to Renal Replacement therapy (RRT). The majority of studies have been unable to account for change in FGF23 over time and those which have demonstrate conflicting results. We performed a survival analysis looking at change in c-terminal FGF23 (cFGF23) over time to assess the relative contribution of cFGF23 to these outcomes.MethodsWe measured cFGF23 on plasma samples from 388 patients with CKD 3-5 who had serial measurements of cFGF23, with a mean of 4.2 samples per individual. We used linear regression analysis to assess the annual rate of change in cFGF23 and assessed the relationship between time-varying cFGF23 and the outcomes in a cox-regression analysis.ResultsAcross our population, median baseline eGFR was 32.3mls/min/1.73m2, median baseline cFGF23 was 162 relative units/ml (RU/ml) (IQR 101-244 RU/mL). Over 70 months (IQR 53-97) median follow-up, 76 (19.6%) patients progressed to RRT, 86 (22.2%) died, and 52 (13.4%) suffered a major non-fatal CV event. On multivariate analysis, longitudinal change in cFGF23 was significantly associated with risk for death and progression to RRT but not non-fatal cardiovascular events.ConclusionIn our study, increasing cFGF23 was significantly associated with risk for death and RRT.
Highlights
Fibroblast growth factor23 (FGF23) is elevated in CKD and has been associated with outcomes such as death, cardiovascular (CV) events and progression to Renal Replacement therapy (RRT)
Our study examined c-terminal FGF23 (cFGF23) levels over time in a cohort of 388 patients selected from the Salford Kidney Study (SKS) to analyse the relationship between change in cFGF23 and the clinical outcomes of death, renal progression and cardiovascular events
We investigated the relationship between change in cFGF23 over time and risk for death, progression to RRT and cardiovascular events
Summary
Fibroblast growth factor (FGF23) is elevated in CKD and has been associated with outcomes such as death, cardiovascular (CV) events and progression to Renal Replacement therapy (RRT). Recognition of FGF23 as an important pathological factor in CKD has made it a prime biomarker to investigate in clinical studies and a potential target for future therapeutic intervention [3, 4]. Numerous studies have investigated the relationship between baseline FGF23 and clinical outcomes in CKD. FGF23 has been shown to associate with risk for death [5,6,7,8,9,10] and cardiovascular events [7, 9, 11,12,13] in both dialysis and non-dialysis populations. High FGF23 impairs host defense in mice and CKD patients [23], increasing risk of infection related hospitalizations in older adults [24]
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