INTRODUCTION: Chronic hemodialysis (HD) patients have bad prognosis and cardiovascular diseases (CVD) represent their main threatening complication. Fibroblast growth factor (FGF-23) has been associated with all kinds of evil consequences, including cardiovascular morbidity, but some studies demonstrated the contrary. Therefore, it is important to know whether FGF-23 is associated with cardiovascular risk or protection. The purpose of this study was to assess the links between FGF-23 and intimal vascular calcification (VC) and with the presence of CVD in chronic HD patients. PATIENTS AND METHODS: This study was carried out on a cohort of randomly selected 88 prevalent HD patients. We recorded demographical, clinical, and biochemical data, including FGF-23. VC was evaluated on carotid ultrasound. CVD were registered. RESULTS: The mean age was 59.68 ± 14.49 years, HD vintage was 59.61 ± 52.39 months, and 20 patients were diabetic (22.72 %). VC was present in 54 patients (61.4 %) and 25 patients (28.4 %) had CVD. FGF-23 correlated positively with HD vintage (r = 0.37; p < 0.001) and iPTH (r = 0.21; p = 0.048). FGF-23 did not correlate with VC score. Patients with CVD were older (p = 0.006), had lower FGF-23 (p = 0.008), higher VC score (p = 0.009), lower Hb (p = 0.008), albumin (p = 0.003), and creatinine (p = 0.03). Low FGF-23 was identified as a risk factor for CVD. CONCLUSION: We report on a novel association between low FGF23 and CVD in chronic HD patients and a lack of correlation of FGF-23 with VC. FGF-23 could play a role in cardiovascular protection that remains to be confirmed in larger studies.
INTRODUCTION: Chronic hemodialysis (HD) patients have bad prognosis and cardiovascular diseases (CVD) represent their main threatening complication. Fibroblast growth factor (FGF-23) has been associated with all kinds of evil consequences, including cardiovascular morbidity, but some studies demonstrated the contrary. Therefore, it is important to know whether FGF-23 is associated with cardiovascular risk or protection. The purpose of this study was to assess the links between FGF-23 and intimal vascular calcification (VC) and with the presence of CVD in chronic HDpatients. PATIENTS AND METHODS: This study was carried out on a cohort of randomly selected 88 prevalent HDpatients. We recorded demographical, clinical, and biochemical data, including FGF-23. VC was evaluated on carotid ultrasound. CVD were registered. RESULTS: The mean age was 59.68 ± 14.49 years, HD vintage was 59.61 ± 52.39 months, and 20 patients were diabetic (22.72 %). VC was present in 54 patients (61.4 %) and 25 patients (28.4 %) had CVD. FGF-23 correlated positively with HD vintage (r = 0.37; p < 0.001) and iPTH (r = 0.21; p = 0.048). FGF-23 did not correlate with VC score. Patients with CVD were older (p = 0.006), had lower FGF-23 (p = 0.008), higher VC score (p = 0.009), lower Hb (p = 0.008), albumin (p = 0.003), and creatinine (p = 0.03). Low FGF-23 was identified as a risk factor for CVD. CONCLUSION: We report on a novel association between low FGF23 and CVD in chronic HDpatients and a lack of correlation of FGF-23 with VC. FGF-23 could play a role in cardiovascular protection that remains to be confirmed in larger studies.
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