title: Vitamin D receptor agonist supplementation and suppression of inflammation may have advantage for all-cause mortality in hemodialysis patients.
abstract: BACKGROUND
  Vitamin D deficiency is common in hemodialysis (HD) patients. The aim of this study was to determine whether HD patients with low 25-hydroxyvitamin D [25(OH)D] levels are at increased risk of mortality.
  
  
  METHODS
  This was a prospective cohort study of Japanese HD patients. We selected all patients with measured serum 25(OH)D levels at the time of entry. We assessed the impact of low serum 25(OH)D levels on the long-term mortality of HD patients by performing Cox regression analyses. Associations between serum 25(OH)D levels and all-cause mortality were also investigated.
  
  
  RESULTS
  Data from 100 patients (mean age 61.0 ± 11.8 years, 64 % males) were available. There was a high prevalence (55 %) of 25(OH)D insufficiency < 20 ng/ml, and 51 % of study subjects were treated with alfacalcidol. Twenty-four patients died during a follow-up period of 4.6 years. There were no significant associations between serum 25(OH)D levels and all-cause mortality (p = 0.777). After adjustments for possible confounders, the hazard ratio (with 95 % CI) for all-cause mortality was 1.091 (1.024-1.167) for age, 0.734 (0.566-1.167) for dialysis vintage, 1.012 (0.995-1.031) for serum total cholesterol values, 2.028 (1.093-3.701) for serum phosphate levels, and 0.291 (0.088-0.855) for treatment with alfacalcidol. A survival advantage of alfacalcidol treatment was observed (log-rank, p = 0.0150). The group of subjects whose serum (25(OH)D level was <20 ng/ml and who were not treated with alfacalcidol had the highest mortality rate.
  
  
  CONCLUSIONS
  Vitamin D deficiency in HD patients who had not taken vitamin D receptor agonist (VDRA) is associated with an increased risk of all-cause mortality. VDRA supplementation may suppress chronic inflammation and have some advantage for mortality of HD patients with vitamin D deficiency.
authors.affiliation: Department of Medicine, Medical Center East, Tokyo Women's Medical University, 2-1-10 Nishiogu, Arakawa-ku, Tokyo 116-8567, Japan.
authors.forename: Tetsuya
authors.initials: T
authors.lastname: Ogawa
authors.forename: Ai
authors.initials: A
authors.lastname: Kyono
authors.forename: Masayo
authors.initials: M
authors.lastname: Sato
authors.forename: Himiko
authors.initials: H
authors.lastname: Sugimoto
authors.forename: Kuniaki
authors.initials: K
authors.lastname: Otsuka
authors.forename: Kosaku
authors.initials: K
authors.lastname: Nitta
mesh_terms: D000368:Aged; D015331:Cohort Studies; D005260:Female; D006801:Humans; D006887:Hydroxycholecalciferols / Q000627:therapeutic use*; D007249:Inflammation / Q000188:drug therapy*; D007676:Kidney Failure, Chronic / Q000401:mortality; D008297:Male; D008875:Middle Aged; D011446:Prospective Studies; D018167:Receptors, Calcitriol / Q000819:agonists*; D006435:Renal Dialysis / Q000401:mortality; D014807:Vitamin D / Q000031:analogs & derivatives / Q000097:blood; D014808:Vitamin D Deficiency / Q000150:complications*
chemical_list: D006887:Hydroxycholecalciferols; D018167:Receptors, Calcitriol; D014807:Vitamin D; C104450:25-hydroxyvitamin D; C008088:alfacalcidol