Mineral Metabolism and Arterial Functions in End-Stage Renal Disease: Potential Role of 25-Hydroxyvitamin D Deficiency

Abstract

In ESRD, arterial function is abnormal, characterized by decreased capacitive function (arterial stiffening) and reduced conduit function, shown by diminished flow-mediated dilation (FMD). The pathophysiology of these abnormalities is not clear, and this cross-sectional study analyzed possible relationships among arterial alterations and cardiovascular risk factors, including mineral metabolism parameters, such as serum parathormone, and vitamin D “nutritional” and “hormonal” status by measuring serum 25-hydroxyvitamin D [25(OH)D₃] and 1,25-dihydroxyvitamin D₃ [1,25(OH)₂D₃] levels. Aortic stiffness (pulse wave velocity), brachial artery (BA) distensibility (echotracking; n = 42), BA FMD (hand-warming; n = 37), and arterial calcification scores (echography and plain x-rays) were measured in 52 stable and uncomplicated patients who were on hemodialysis. 25(OH)D₃ and 1,25(OH)₂D₃ serum levels were low and weakly correlated (r = 0.365, P < 0.05). After adjustment for BP and age, multivariate analyses indicated that 25(OH)D₃ and 1,25(OH)₂D₃ were negatively correlated with aortic pulse wave velocity (P < 0.001) and positively correlated with BA distensibility (P < 0.01) and FMD (P < 0.001). Arterial calcification scores were not independently associated with 25(OH)D₃ and 1,25(OH)₂D₃ serum concentrations. These results suggest that nutritional vitamin D deficiency and low 1,25(OH)₂D₃ could be associated with arteriosclerosis and endothelial dysfunction in patients who have ESRD and are on hemodialysis.