Ergocalciferol treatment does Not improve erythropoietin utilization and hospitalization rate in hemodialysis patients

Abstract

Background: Vitamin D (25-hydroxyvitamin D; 25[OH]D) deficiency (VDD) is highly prevalent in chronic kidney disease. The aim of this study was to evaluate the effect of oral ergocalciferol supplementation on requirement of erythropoietin (EPO) and active vitamin D analogues, and hospitalization rate in maintenance hemodialysis (HD) patients.Methods: This retrospective cohort study included 186 patients who were on HD for 3 months and had 25(OH)D levels < 30 ng/ml. Over 1-year period, 107 patients were supplemented with protocol-based ergocalciferol (D 2 group) and 79 were not (control). Parameters of erythropoiesis and bone-mineral metabolism, and monthly doses of EPO and paricalcitol were assessed at 6-and 12-months of ergocalciferol supplementation. Total hospitalizations were recorded for the same year. Results: Baseline characteristics were similar across two arms except higher serum ferritin, transferrin saturation and prevalence of stroke in D2 and higher coronary artery disease in control group with overall mean ± SD 25(OH)D level of 16.8 ± 7 ng/ml. At 12 months, 25(OH)D levels increased significantly in D 2 group compared to control (30.5 ± 11.7 vs. 14.2 ± 9.3 ng/ml; p < 0.001). The EPO dose remained same with no difference in hemoglobin values between the two groups during the intervention period. On multivariate regression which included above variables there was no effect of ergocalciferol treatment on EPO dose (p = ns). Hospitalization rate was similar in two arms; however, ergocalciferol treatment inversely associated with paricalcitol dose (β ± SE = −10. 4 ± 2.8; p < 0.001). Conclusions: One-year of ergocalciferol supplementation was not associated with reduction in EPO requirement or hospitalization rate in HD patients with VDD. Further studies are warranted to determine definitive role of nutritional vitamin D in these patients.

Vitamin D supplementation on anemia markers and the impact on PTH in patients with chronic kidney disease

“…Vitamin D supplementation culminated in a significant decrease in PTH levels, as reported in Nand and Mittal (2017) and Matias et al (2010), in Kumar et al (2011), Porter et al (2013, Miskulin et al (2016), Agarwal et al (2016) and Obi et al (2020) no significant difference was found in PTH levels.…”

“…In turn, Nand and Mittal (2017) found a reduction in the dose of EPO and an increase in hemoglobin levels with cholecalciferol supplementation. Agarwal et al (2016), Miskulin et al (2016) and Obi et al (2020) found no significant difference between the groups regarding the dose of EPO, epoetin and darbepoetin, respectively.…”

“…Although the study designs are different, they were all based on interventions with vitamin D supplementation. Matias et al (2010), Kumar et al (2011), Naini et al (2015, Agarwal et al (2016) and Obi et al (2020) observed an increase in the concentration of 25(OH)D2 with vitamin D supplementation. Porter et al (2013) found an oscillation in the concentration of 25(OH)D2; at 6 months of treatment there was a significant increase, and 11 months after the 25(OH)D2 concentration decreased, with only 37% of the case group maintaining an adequate level.…”

Association of erythropoietin resistance and fibroblast growth factor 23 in dialysis patients: Results from the Japanese Dialysis Outcomes and Practice Patterns Study

“…36 Vitamin D supplementation had no effect on ESA dose in vitamin D deficient haemodialysis patients. 37,38 The underlying mechanism among CKD-MBD, anaemia and ESA hyporesponsiveness is not well understood. Since FGF23 is associated with both CKD-MBD and anaemia, FGF23 may be the factor which connects them.…”

“…On the other hand, treatment with active vitamin D in haemodialysis patients with secondary hyperparathyroidism increased FGF23 levels 36 . Vitamin D supplementation had no effect on ESA dose in vitamin D deficient haemodialysis patients 37,38 . The underlying mechanism among CKD‐MBD, anaemia and ESA hyporesponsiveness is not well understood.…”