Intravenous Vitamin B6 Increases Resistance to Erythropoiesis-Stimulating Agents in Hemodialysis Patients: A Randomized Controlled Trial

Objective Vitamin B6 deficiency is common in hemodialysis patients and may contribute to anemia and abnormal bone metabolism in this population. Design 6-month, open-label, randomized controlled parallel-group study in hemodialysis centers. Subjects Fifty-six maintenance hemodialysis patients with relatively high resistance to erythropoiesis-stimulating agents (ESA). Intervention Intravenous vitamin B6 (60 mg of intravenous pyridoxal 5′-phosphate after each thrice-weekly hemodialysis session). Main Outcome Measure The primary and secondary outcomes were changes over time in ESA resistance index and bone turnover markers, respectively. Results The prevalence of vitamin B6 deficiency was 40% overall. Compared with the control group, the B6 group showed an upward change in ESA resistance index over time ( P interaction  = .038). At week 13 (a priori–defined time point), pyridoxal 5′-phosphate administration was associated with higher ESA resistance index by 0.97 (95% confidence interval, 0.02-1.92) ×10 −2  μg ⋅darbepoetin-α/kg per g/dL⋅hemoglobin after baseline adjustment, which was not modified by baseline vitamin B6 status. There was a trend toward increase in serum erythropoietin concentrations in the B6 group after adjustment for baseline values, hemoglobin, and weekly ESA dose ( P interaction  = .06). The downward changes of bone-specific alkaline phosphatase and tartrate-resistant acid phosphatase 5b in the B6 group relative to the control group were pronounced in patients without vitamin B6 deficiency ( P interaction Conclusions Thrice-weekly intravenous vitamin B6 (60 mg pyridoxal 5′-phosphate hydrate) worsens the response to ESA and may blunt the response of bone to parathyroid hormone in hemodialysis patients.