Vitamin D Treatment Effect on Serum Endocan and High-Sensitivity C-Reactive Protein Levels in Renal Transplant Patients

Atis O. , KELEŞ M., ÇANKAYA E. , DOĞAN H. , Aksoy H., Akcay F.

PROGRESS IN TRANSPLANTATION, vol.26, no.4, pp.335-339, 2016 (Journal Indexed in SCI) identifier identifier identifier

  • Publication Type: Article / Article
  • Volume: 26 Issue: 4
  • Publication Date: 2016
  • Doi Number: 10.1177/1526924816664086
  • Page Numbers: pp.335-339


Context: Endocan is a marker showing endothelial dysfunction and inflammation. Significantly increased endocan levels have been observed in serum of patients with sepsis and cancer. Objective: Our aim was to investigate the relationship between vitamin D treatment and serum endocan and high-sensitivity C-reactive protein (hs-CRP) levels as inflammatory markers in transplant patients. Design: Prospective. Setting: Nephrology clinic. Patients: Thirty-eight renal transplant patients with serum 25-hydroxy-vitamin D (25-OH-vitamin D) levels below 20 ng/ mL and transplanted at least 12 months. Intervention: One-time oral dose of 300 000 IU vitamin D3. Main Outcome Measures: Before and after vitamin D treatment, serum endocan, hs-CRP, calcium, phosphorus, and parathyroid hormone (PTH) levels were measured. Results: Median serum endocan and PTH values before vitamin D were significantly higher than those of after treatment values (P = .001 and P < .001, respectively). On the other hand, serum total calcium and phosphorus levels before vitamin D treatment were lower than the values obtained after vitamin D treatment (P = .0013 and P < .001, respectively). Serum hs-CRP was lower after vitamin D therapy than before, but the difference was not statistically significant (P = .06). A moderate negative correlation was determined between endocan and 25-OH-vitamin D levels after treatment with vitamin D (r =-.36, P = .02). Conclusion: This study has revealed that vitamin D treatment reduced markers of endothelial dysfunction in patients with renal transplantation and vitamin D deficiency.