title: Vitamin D, vitamin D receptor and the importance of its activation in patients with chronic kidney disease.
abstract: Vitamin D deficiency has been linked to many different pathologies, especially with morbimortality in patients with chronic kidney disease. The progressive loss of renal function leads to calcitriol deficiency and homeostatic changes in calcium, phosphorus, FGF-23 and PTH, among others. All these changes can also influence vitamin D receptor (VDR) activation and the development of secondary hyperparathyroidism (SHPT). The biologic actions of both vitamin D and its synthetic analogues are mediated by binding to the same VDR, acting on different genes. There is a narrow relationship between low levels of calcitriol and SHPT. The combined approach of VDR activation and phosphate restriction, among others, plays an important role in the early treatment of the chronic kidney disease-mineral and bone disorder (CKD-MBD). The Spanish Society of Nephrology, in order to reduce the uniform and significant association with CKD-associated mortality, calcidiol and high phosphate levels suggests normalization of phosphate as well as calcidiol levels in both CKD and dialysis patients. Moreover, it considers that, in addition to selective/non selective activation of VDR for the prevention and treatment of SHPT, VDR could be activated in dialysis patients by native vitamin D or even low paricalcitol doses, independently of PTH levels, as some cohort studies and a recent metaanalysis have found an association between treatment with active vitamin D and decreased mortality in patients with CKD. In general it is considered reasonable to use all this information to individualise decision making.
authors.forename: Jordi
authors.initials: J
authors.lastname: Bover
authors.forename: Jesús
authors.initials: J
authors.lastname: Egido
authors.forename: Elvira
authors.initials: E
authors.lastname: Fernández-Giráldez
authors.forename: Manuel
authors.initials: M
authors.lastname: Praga
authors.forename: Carlos
authors.initials: C
authors.lastname: Solozábal-Campos
authors.forename: José V
authors.initials: JV
authors.lastname: Torregrosa
authors.forename: Alberto
authors.initials: A
authors.lastname: Martínez-Castelao
mesh_terms: D000818:Animals; D002112:Calcifediol / Q000097:blood; D057966:Calcimimetic Agents / Q000627:therapeutic use; D002117:Calcitriol / Q000627:therapeutic use; D012080:Chronic Kidney Disease-Mineral and Bone Disorder / Q000188:drug therapy / Q000209:etiology*; D002986:Clinical Trials as Topic; D004353:Drug Evaluation, Preclinical; D057915:Drug Substitution; D004872:Ergocalciferols / Q000494:pharmacology / Q000627:therapeutic use*; D000089703:Fibroblast Growth Factor-23; D006801:Humans; D006962:Hyperparathyroidism, Secondary / Q000188:drug therapy / Q000209:etiology; D010710:Phosphates / Q000097:blood; D051381:Rats; D018167:Receptors, Calcitriol / Q000819:agonists / Q000502:physiology*; D006435:Renal Dialysis; D051436:Renal Insufficiency, Chronic / Q000150:complications* / Q000378:metabolism; D014807:Vitamin D / Q000502:physiology* / Q000627:therapeutic use
chemical_list: D057966:Calcimimetic Agents; D004872:Ergocalciferols; C000717427:FGF23 protein, human; D010710:Phosphates; D018167:Receptors, Calcitriol; C579457:VDR protein, human; D014807:Vitamin D; C084656:paricalcitol; D000089703:Fibroblast Growth Factor-23; D002117:Calcitriol; D002112:Calcifediol