International Journal of Endocrinology · 2015 · 30 citations · 39 references
MedicineCardiologyEndocrinologyCalcium HomeostasisMicronutrient NutritionRenal PathophysiologyChronic Kidney DiseaseDiabetic Kidney DiseaseMagnesium DeficiencyMagnesium HomeostasisMitral Valve DiseaseRenal DiseaseCardiovascular Disease MortalityCardiovascular Risk MarkersFibroblast Growth Factor 23 DysregulationMagnesium ConcentrationMitral Valve CalcificationValve Calcification AssessmentValvular CalcificationWilkins Scoring
Background. Mitral valve calcification and intima media thickness (IMT) are common complications of chronic kidney disease (CKD) implicated with high cardiovascular mortality. Objective. To investigate the implication of magnesium and fibroblast growth factor-23 (FGF-23) levels with mitral valve calcification and IMT in CKD diabetic patients. Methods. Observational, prospective study involving 150 diabetic patients with mild to moderate CKD, divided according to Wilkins Score. Carotid-echodoppler and transthoracic echocardiography were used to assess calcification. Statistical tests used to establish comparisons between groups, to identify risk factors, and to establish cut-off points for prediction of mitral valve calcification. Results. FGF-23 values continually increased with higher values for both IMT and calcification whereas the opposite trend was observed for magnesium. FGF-23 and magnesium were found to independently predict mitral valve calcification and IMT (P < 0.05). Using Kaplan-Meier analysis, the number of deaths was higher in patients with lower magnesium levels and poorer Wilkins score. The mean cut-off value for FGF-23 was 117 RU/mL and for magnesium 1.7 mg/dL. Conclusions. Hypomagnesemia and high FGF-23 levels are independent predictors of mitral valve calcification and IMT and are risk factors for cardiovascular mortality in this population. They might be used as diagnostic/therapeutic targets in order to better manage the high cardiovascular risk in CKD patients.
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Medicine, Endocrinology, Nutrition +17
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