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Comparison of calcium acetate and sevelamer on vascular function and fibroblast growth factor 23 in CKD patients: a
Mahmut Ilker Yilmaz1, Alper Sonmez, Mutlu Saglam
1Department of Nephrology, Gülhane School of Medicine, Etlik-Ankara, Turkey. mahmutiyilmaz@yahoo.com
Insights
In patients with stage 4 chronic kidney disease (CKD), phosphate binders improved vascular function. Fibroblast growth factor 23 (FGF-23) levels changed with treatment, suggesting FGF-23 may impact vascular dysfunction independently of phosphate levels.
Area of Science:
- Nephrology
- Cardiovascular Medicine
- Endocrinology
Background:
- Fibroblast growth factor 23 (FGF-23) is linked to endothelial dysfunction and atherosclerosis in chronic kidney disease (CKD).
- Previous research suggests phosphate binders may influence FGF-23 and endothelial function beyond phosphate reduction.
- This study investigated sevelamer versus calcium acetate effects on vascular function and FGF-23.
Purpose of the Study:
- To compare the effects of sevelamer and calcium acetate on vascular function in patients with stage 4 CKD.
- To assess the impact of these treatments on FGF-23 levels.
- To explore the relationship between FGF-23 changes and vascular function improvements.
Main Methods:
- A randomized prospective open-label trial involving 100 patients with stage 4 CKD and hyperphosphatemia.
- An 8-week intervention comparing sevelamer (n=47) and calcium acetate (n=53).
- Primary outcome: change in flow-mediated vasodilatation; Secondary outcome: change in FGF-23 levels.
Main Results:
- Both treatments reduced serum phosphate, with a more significant decrease in the sevelamer group.
- Flow-mediated vasodilatation increased significantly with sevelamer but not with calcium acetate.
- Changes in flow-mediated vasodilatation correlated with FGF-23 level changes, independent of phosphate reduction.
Conclusions:
- Phosphate lowering in stage 4 CKD patients improves flow-mediated vasodilatation.
- FGF-23 level changes induced by phosphate binders are associated with vascular function changes, irrespective of phosphate levels.
- These findings support the hypothesis that FGF-23 may contribute to vascular dysfunction in CKD patients.
Background:
Fibroblast growth factor 23 (FGF-23) is a marker of endothelial dysfunction and atherosclerotic complications in patients with chronic kidney disease (CKD). Because previous studies suggested that sevelamer may exert effects on FGF-23 level and endothelial function independently of its phosphate-lowering action, we tested the effect of sevelamer versus calcium acetate on vascular function and FGF-23 levels.
Study Design:
Randomized prospective open-label trial.
Setting & Participants:
Patients with stage 4 CKD with hyperphosphatemia (n = 100).
Intervention:
An 8-week intervention with sevelamer (n = 47) and calcium acetate (n = 53).
Outcomes:
The primary study outcome was change in flow-mediated vasodilatation in the forearm. The secondary outcome was change in FGF-23 levels.
Results:
Serum phosphate levels decreased in both treatment arms (P < 0.001), but more markedly in the sevelamer group (P < 0.001). Flow-mediated vasodilatation increased from 6.1% to 7.1% (P < 0.001) in sevelamer-treated patients, whereas it was unchanged in the calcium-acetate group (6.0% vs 6.0%). In a combined analysis, treatment-induced changes in flow-mediated vasodilatation were (P < 0.001) associated with simultaneous changes in FGF-23 levels (-27.1% [-33.2% to -8.8%] for the sevelamer group; 3.5% [-8.4% to 12.1%] for the calcium acetate group), as well as with C-reactive protein and fetuin A levels. These relationships were confirmed in multiple regression analysis adjusting for changes in serum phosphate levels and other factors.
Limitations:
Unblinded randomized controlled study that cannot establish mechanisms of effect.
Conclusions:
In hyperphosphatemic patients with stage 4 CKD, treatment with phosphate lowering induces measurable improvements in flow-mediated vasodilatation. Furthermore, independently of serum phosphate level, FGF-23 level changes induced by phosphate binders are associated with simultaneous changes in flow-mediated vasodilatation. These observations are compatible with the hypothesis that FGF-23 may contribute to vascular dysfunction in this population.
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