In patients on hemodialysis, as in the general population, poor vitamin D status is associated with increased vascular risk, possibly reflecting a role for vitamin D in control of PTH [124]. Despite inefficient conversion of 25-hydroxyvitamin D to calctriol in patients on hemodialysis, vitamin D supplementation in adequate amounts (preferably as the natural agent cholecalciferol [125]) can indeed support calcitriol production and down-regulate PTH [126–128]. Alternatively, more direct-acting pharmaceutical vitamin D agonists such as alfacalcidol, calcitriol, and paricalcitol can be expected to have a more substantial impact on PTH in patients on hemodialysis, but these agents have the potential to increase phosphate and calcium absorptiondalbeit paricalcitol seems to pose less risk in this regard [129]. Observational studies suggest that low-dose alfacalcidol improves survivaldhighlighting the pathogenic effect of secondary hyperparathyroidism in renal failure [130–132].