The Relationship Between Arterial Stifness and 25-(Oh) Vitamin D, FGF 23 in Maintenance Hemodialysis Patients

Abstract

AIM: Vascular calcification (VC) is highly prevalent in maintenance hemodialysis (MHD) population and increasing evidence indicates that abnormalities in mineral metabolism are closely associated with VC and increased mortality in chronic kidney disease (CKD) patients. In our study, we aimed to determine whether high Fibroblast growth factor-23 (FGF-23) and low 25 (OH) Vitamin D levels are a result of high calcium load and whether there is a relationship between 25 (OH) Vitamin D levels and arterial stiffness in CKD patients. MATERIAL AND METHODS:One hundred and seventeen patients who were receiving MHD 3 times a week for at least 24 months were selected and followed up for 12 months and laboratory results were recorded from patient files. We analyzed the influence of a yearlong cumulative calcium and therapeutic vitamin D (paricalcitol and calcitriol) intake and serum FGF-23 level on endogenous 25(OH)D levels and the impacts of these parameters on the change in annual pulse wave velocity (PWV) measurement results in MHD patients. RESULTS:Elementary calcium dose was significantly higher in vitamin D insufficiency group than control group (P=0.014). Serum levels of FGF-23 were positively correlated with duration of HD (P=0.001), mean parathyroid hormone (PTH) (P=0.001), mean phosphorus (P) (P=0.009) and mean CaXP (P=0.006). Baseline PWV measurement were similar between two groups, however patients in insufficiency group had higher 12th month PWV measurements compared to control group (P=0.034). CONCLUSION:Calcium could increase serum FGF23 levels by indeterminate mechanisms independently of serum phosphorus level. Additionally, elevated FGF-23 level was found to be insulting a decline in vitamin D levels which may cause VC and stiffening of the arteries and resulting higher PWV measurements.