For a long time, the role of vitamin D in chronic kidney disease (CKD) received less attention than treating vitamin D metabolism disorders.
Low active vitamin D levels represent one of the most important factors in the pathophysiology of secondary hyperparathyroidism. For this reason, the administration of active vitamin D compounds is commenced during the course of CKD treatment. Moreover, patients with CKD exhibit a high prevalence of hypovitaminosis of 25-hydroxyvitamin D (25[OH]D) unrelated to vitamin D intake.
However, several studies have recently advanced our knowledge about the effects of both the 25(OH) D and 1,25(OH)2D forms of endogenous vitamin D and the possible beneficial effects of vitamin D treatment. These studies add to the already well-known effects of vitamin D on mineral metabolism. Several studies have hypothesized a link between reduced levels of 25-OH D and a greater cardiovascular risk in the general population.
Another important aspect of vitamin D metabolism is the existence of polymorphic genetic variants of the vitamin D receptors (VDRs). Most studies have aimed to determine whether VDR polymorphisms are involved in the development of secondary hyperparathyroidism (sHPT).