VITAMIN D DEFICIENCY, BONE TURNOVER MARKERS AND ARTERIAL CALCIFICATIONS IN NON-DIALYSIS CHRONIC KIDNEY DISEASE PATIENTS.

INTRODUCTION

Vitamin D [25(OH)D] deficiency is prevalent in chronic kidney disease (CKD), related to bone turnover and potentially involved in arterial calcifications.

OBJECTIVE

To evaluate vitamin D status in non-dialysis CKD patients and its relationships with bone turnover markers (BTM) and arterial calcifications.

DESIGN

Cross-sectional, prospective, multicentric study.

SUBJECTS AND METHODS

One hundred twenty-eight CKD patients (median age 61 years, 58% males, median eGFR 29mL/min) were included. Comorbidities, mineral and bone metabolism parameters were evaluated. Total alkaline phosphatase (T-ALP) was used to assess bone turnover. Atherosclerosis was evaluated by carotid intima-media thickness (CIMT), endothelial calcifications by aortic calcification score (ACS), and arterial stiffness by cardio-ankle vascular index (CAVI). Vitamin D deficiency was defined as 25(OH)D <15 ng/mL. Factors associated with vitamin D, T-ALP and vascular parameters were assessed in multivariate regression models.

RESULTS

Prevalence of vitamin D deficiency was 63% and median 25(OH)D was 12.8 ng/mL. Older age, female sex and higher parathormone were predictors of vitamin D deficiency. Increased T-ALP was predicted by higher parathormone, suggesting high turnover bone disease. While age was a determinant of all evaluated vascular parameters, lower 25(OH)D was associated only with endothelial calcifications, which correlated with CAVI, suggesting a direct relation between vitamin D deficiency mediated plaques calcification and arterial stiffness.

CONCLUSION

Vitamin D deficiency was highly prevalent in this non-dialysis CKD cohort and was related to age, sex and parathormone. Vitamin D deficiency was associated with increased calcifications of endothelial plaques, which seemed to increase arterial stiffness.