Ferric Gluconate Is Highly Efficacious in Anemic Hemodialysis Patients with High Serum Ferritin and Low Transferrin Saturation

Abstract

Few data exist to guide treatment of anemic hemodialysis patients with high ferritin and low transferrin saturation (TSAT).The Dialysis Patients' Response to IV Iron with Elevated Ferritin (DRIVE) trial was designed to evaluate the efficacy of intravenous ferric gluconate in such patients. Inclusion criteria were hemoglobin <11 g/dl, ferritin 500 to 1200 ng/ml, TSAT <25%, and epoetin dosage >225 IU/kg per wk or >22,500 IU/wk. Patients with known infections or recent significant blood loss were excluded. Participants (n ‫؍‬ 134) were randomly assigned to no iron (control) or to ferric gluconate 125 mg intravenously with eight consecutive hemodialysis sessions (intravenous iron). At randomization, epoetin was increased 25% in both groups; further dosage changes were prohibited. At 6 wk, hemoglobin increased significantly more (P ‫؍‬ 0.028) in the intravenous iron group (1.6 ؎ 1.3 g/dl) than in the control group (1.1 ؎ 1.4 g/dl). Hemoglobin response occurred faster (P ‫؍‬ 0.035) and more patients responded after intravenous iron than in the control group (P ‫؍‬ 0.041). Ferritin <800 or >800 ng/ml had no relationship to the magnitude or likelihood of responsiveness to intravenous iron relative to the control group. Similarly, the superiority of intravenous iron compared with no iron was similar whether baseline TSAT was above or below the study median of 19%. Ferritin decreased in control subjects (؊174 ؎ 225 ng/ml) and increased after intravenous iron (173 ؎ 272 ng/ml; P < 0.001). Intravenous iron resulted in a greater increase in TSAT than in control subjects (7.5 ؎ 7.4 versus 1.8 ؎ 5.2%; P < 0.001). Reticulocyte hemoglobin content fell only in control subjects, suggesting worsening iron deficiency. Administration of ferric gluconate (125 mg for eight treatments) is superior to no iron therapy in anemic dialysis patients receiving adequate epoetin dosages and have a ferritin 500 to 1200 ng/ml and TSAT <25%.

Ferric Gluconate Reduces Epoetin Requirements in Hemodialysis Patients with Elevated Ferritin

“…[1][2][3] The 2006 anemia guidelines by the National Kidney Foundation Kidney Disease Outcomes Quality Initiative recommend that dose of ESA be considered as one of several factors when deciding to administer intravenous iron to patients. 10 The Dialysis Patients Response to IV Iron with Elevated Ferritin (DRIVE) study was a randomized controlled trial that showed that intravenous ferric gluconate was effective in improving anemia in hemodialysis patients with ferritin of 500 to 1200 ng/ml, transferrin saturation (TSAT) Յ 25%, and adequate epoetin doses, 11 disproving the widely held belief that patients with ferritin more than 500 ng/ml are unlikely to benefit from intravenous iron administration. 10,12,13 In the context of an increased epoetin dose, intravenous ferric gluconate patients were more likely to mount a hematologic response than controls, regardless of baseline levels of ferritin, TSAT, C-reactive protein, Hb, soluble transferrin receptor, epoetin dose, or reticulocyte Hb content.…”

Receipt of Intravenous Iron and Clinical Outcomes among Hemodialysis Patients Hospitalized for Infection

“…In an international prospective cohort of hemodialysis patients, a nonlinear association between intravenous iron and infection-related mortality was observed, wherein patients prescribed no iron or doses $200 mg per month were at nonstatistically significantly higher risk compared with patients prescribed lower-dose intravenous iron (17). Two small randomized trials involving iron repletion in hemodialysis patients collected data about infectious outcomes as part of their safety analysis and did not find a difference in infectious adverse events between the intervention and control groups (18,19). Estimated adjusted association and length of stay data are presented with 95% confidence intervals.…”

Eisenmangel, Thrombozytose und Thromboembolie

“…Eine Behandlung mit Erythropetin und Analoga ist der Eckpfeiler der Therapie der renalen Anämie. Paradoxerweise führt aber eine Normalisierung des Hämoglobins mittels Erythropoese-stimulierenden Agenten zu einer erhöhten Morbidität und Mortalität [73][74][75][76] [80,81], und eine adäquate Eisenzufuhr kann die Plättchenanzahl wieder normalisieren [79]. Ein unbehandelter Eisenmangel erhöht die Mortalität bei Patienten mit chronischer Niereninsuffizienz [82,83].…”