A randomized controlled trial comparing intravenous ferric carboxymaltose with oral iron for treatment of iron deficiency anaemia of non-dialysis-dependent chronic kidney disease patients

Abstract

Background. Iron deficiency is a common cause of anaemia and hyporesponsiveness to erythropoiesis-stimulating agents (ESAs) in non-dialysis-dependent chronic kidney disease (ND-CKD) patients. Current intravenous iron agents cannot be administered in a single high dose because of adverse effects. Ferric carboxymaltose, a non-dextran parenteral iron preparation, can be rapidly administered in high doses.Methods. This open-label trial randomized 255 subjects with glomerular filtration rates ≤ 45 mL/min/1.73 m2, haemoglobin ≤ 11 g/dL, transferrin saturation ≤ 25%, ferritin ≤ 300 ng/mL, and stable ESA dose to either intravenous ferric carboxymaltose 1000 mg over 15 min (with up to two additional doses of 500 mg at 2-week intervals) or oral ferrous sulphate 325 mg thrice daily for a total of 195 mg elemental iron daily for 56 days.Results. In the modified intent-to-treat population, the proportion of subjects achieving a haemoglobin increase ≥ 1 g/dL at any time was 60.4% with ferric carboxymaltose and 34.7% with oral iron (P < 0.001). At Day 42, mean increase in haemoglobin was 0.95 ± 1.12 vs 0.50 ± 1.23 g/dL (P = 0.005), mean increase in ferritin was 432 ± 189 ng/mL vs 18 ± 45 ng/mL (P < 0.001) and mean increase in transferrin saturation was 13.6 ± 11.9% vs 6.1 ± 8.1% (P < 0.001). Treatment-related adverse events were significantly fewer with ferric carboxymaltose than with oral iron (2.7% and 26.2%, respectively; P < 0.0001).Conclusions. We conclude that 1000 mg ferric carboxymaltose can be rapidly administered, is more effective and is better tolerated than oral iron for treatment of iron deficiency in ND-CKD patients.

Intravenous Iron Is Effective and Safe in Correcting Anemia in Erythropoietin-Treated Hemodialysis Patients

“…This study is consistent with other studies that showed that in iron deficient hemodialysis patients randomized to oral iron or intravenous iron, only the group treated with intravenous iron had a significant increase in hemoglobin levels [9][10][11][12]. Intravenous iron preparations have very different molecular weights and side effect profiles [13], small proportions of patients given intravenous iron dextran develop a lifethreatening anaphylactic reaction, which is due to an immune-mediated reaction in patients who have dextran antibodies [14].…”

Hepcidin levels predict nonresponsiveness to oral iron therapy in patients with iron deficiency anemia

“…An increase in hepcidin would be expected if oral iron therapy resulted in increased iron stores. That this did not occur in the oral iron group demonstrated an inferior increment in iron stores when compared to FCM therapy [21]. FCM also increased hemoglobin levels significantly when compared to oral iron therapy.…”

Comparing the safety and efficacy of intravenous iron sucrose and intravenous ferric carboxymaltose in treating postpartum anemia

“…Efficacy and safety of FCM has been proved in many clinical trials done so far in patients with varying etiologies of anaemia like, inflammatory bowel disease chronic kidney disease congestive heart failure, heavy uterine bleeding and PPIDA. [8][9][10][11][12][13][14][15][16][17][18] FCM injection leads to Hb rise along with replenishment of iron stores in much shorter time. Also, there is better tolerability with low risk of anaphylaxis and other adverse effects.…”