title: Ergocalciferol treatment and aspects of mineral homeostasis in patients with chronic kidney disease stage 4-5.
abstract: BACKGROUND
  Focus on non-classical effects and possible less side effects of treatment with nutritional vitamin D, raises the expectation of possible benefits from treating chronic kidney disease (CKD) patients with ergocalciferol (vitamin D2). Treatment with 1,25(OH)2 vitamin D (calcitriol) induces elevated fibroblast growth factor 23 (FGF23), while epidemiological studies have found positive effects of nutritional and 25(OH)vitamin D on mortality in CKD. Disturbed mineral homeostasis in CKD is correlated to adverse outcome and cardiovascular mortality. The objective was to examine the possible effects of treatment with high doses of ergocalciferol on parameters of mineral homeostasis in predialysis CKD patients.
  
  
  METHODS
  A total of 43 adult patients with CKD stage 4-5, not receiving vitamin D supplementation, were studied, and allocated by simple randomization to either an intervention (n = 26) or a control group (n = 17). The intervention group received ergocalciferol, 50.000 IU/week for 6 weeks. Plasma FGF23, creatinine, parathyroid hormone (PTH), phosphate and ionized calcium were obtained at baseline and after the 6 weeks.
  
  
  RESULTS
  The intervention group had a significant increase in 25(OH)D2 concentration from < 10 to 90 ± 4 nmol/L, while 1,25(OH)2D (62 ± 6 at baseline and 67 ± 6 pmol/L at 6 weeks) remained stable. No changes were seen in the circulating vitamin D concentrations in the control group. After the 6 weeks of treatment no significant changes were seen in concentration of creatinine, phosphate, ionized calcium, PTH and FGF23 remained stable.
  
  
  CONCLUSIONS
  No harmful effects of short-term treatment with high-dose ergocalciferol were observed on markers of mineral homeostasis and FGF23 in CKD patients stage 4-5.
authors.affiliation: University of Copenhagen, Nephrological Department P, Rigshospitalet, Copenhagen, Denmark.
authors.forename: Eva
authors.initials: E
authors.lastname: Gravesen
authors.forename: Jacob
authors.initials: J
authors.lastname: Hofman-Bang
authors.forename: Ewa
authors.initials: E
authors.lastname: Lewin
authors.forename: Klaus
authors.initials: K
authors.lastname: Olgaard
mesh_terms: D000328:Adult; D001842:Bone and Bones / Q000187:drug effects / Q000378:metabolism*; D002118:Calcium / Q000097:blood; D003404:Creatinine / Q000097:blood; D004872:Ergocalciferols / Q000493:pharmacokinetics / Q000627:therapeutic use*; D005260:Female; D000089703:Fibroblast Growth Factor-23; D005346:Fibroblast Growth Factors / Q000097:blood; D006706:Homeostasis; D006801:Humans; D008297:Male; D010281:Parathyroid Hormone / Q000097:blood; D010710:Phosphates / Q000097:blood; D051436:Renal Insufficiency, Chronic / Q000097:blood / Q000188:drug therapy* / Q000401:mortality / Q000473:pathology; D016896:Treatment Outcome; D014815:Vitamins / Q000493:pharmacokinetics / Q000627:therapeutic use*
chemical_list: D004872:Ergocalciferols; C000717427:FGF23 protein, human; D010281:Parathyroid Hormone; D010710:Phosphates; D014815:Vitamins; D005346:Fibroblast Growth Factors; D000089703:Fibroblast Growth Factor-23; D003404:Creatinine; D002118:Calcium