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Intravenous iron versus erythropoiesis-stimulating agents: friends or foes in treating chronic kidney disease anemia?
Adv Chronic Kidney Dis. 2009 Mar; 16(2):143-51.AC

Abstract

Patients with chronic kidney disease (CKD), especially those requiring maintenance hemodialysis treatments, may lose up to 3 g of iron each year because of frequent blood losses. Higher doses of erythropoiesis-stimulating agents (ESAs) may worsen iron depletion and lead to an increased platelet count (thrombocytosis), ESA hyporesponsiveness, and hemoglobin variability. Hence, ESA therapy requires concurrent iron supplementation. Traditional iron markers such as serum ferritin and transferrin saturation ratio (TSAT) (ie, serum iron divided by total iron-binding capacity [TIBC]), may be confounded by non-iron-related conditions. Whereas serum ferritin <200 ng/mL suggests iron deficiency in CKD patients, ferritin levels between 200 and 1,200 ng/mL may be related to inflammation, latent infections, malignancies, or liver disease. Protein-energy wasting may lower TIBC, leading to a TSAT within the normal range, even when iron deficiency is present. Iron and anemia indices have different mortality predictabilities, in that high serum ferritin but low iron, TIBC, and TSAT levels are associated with increased mortality, whereas hemoglobin exhibits a U-shaped risk for death. The increased mortality associated with targeting hemoglobin above 13 g/dL may result from iron depletion-associated thrombocytosis. Intravenous (IV) iron administration may not only decrease hemoglobin variability and ESA hyporesponsiveness, it may also reduce the greater mortality associated with the much higher ESA doses that have been used in some patients when targeting higher hemoglobin levels.

Authors+Show Affiliations

Harold Simmons Center for Kidney Disease Research and Epidemiology, Los Angeles Biomedical Research Institute at Harbor-UCLA Medical Center, Torrance, CA 90502, USA. kamkal@ucla.eduNo affiliation info availableNo affiliation info availableNo affiliation info available

Pub Type(s)

Journal Article
Research Support, N.I.H., Extramural
Research Support, Non-U.S. Gov't
Review

Language

eng

PubMed ID

19233073

Citation

Kalantar-Zadeh, Kamyar, et al. "Intravenous Iron Versus Erythropoiesis-stimulating Agents: Friends or Foes in Treating Chronic Kidney Disease Anemia?" Advances in Chronic Kidney Disease, vol. 16, no. 2, 2009, pp. 143-51.
Kalantar-Zadeh K, Streja E, Miller JE, et al. Intravenous iron versus erythropoiesis-stimulating agents: friends or foes in treating chronic kidney disease anemia? Adv Chronic Kidney Dis. 2009;16(2):143-51.
Kalantar-Zadeh, K., Streja, E., Miller, J. E., & Nissenson, A. R. (2009). Intravenous iron versus erythropoiesis-stimulating agents: friends or foes in treating chronic kidney disease anemia? Advances in Chronic Kidney Disease, 16(2), 143-51. https://doi.org/10.1053/j.ackd.2008.12.008
Kalantar-Zadeh K, et al. Intravenous Iron Versus Erythropoiesis-stimulating Agents: Friends or Foes in Treating Chronic Kidney Disease Anemia. Adv Chronic Kidney Dis. 2009;16(2):143-51. PubMed PMID: 19233073.
* Article titles in AMA citation format should be in sentence-case
TY - JOUR T1 - Intravenous iron versus erythropoiesis-stimulating agents: friends or foes in treating chronic kidney disease anemia? AU - Kalantar-Zadeh,Kamyar, AU - Streja,Elani, AU - Miller,Jessica E, AU - Nissenson,Allen R, PY - 2009/2/24/entrez PY - 2009/2/24/pubmed PY - 2009/4/8/medline SP - 143 EP - 51 JF - Advances in chronic kidney disease JO - Adv Chronic Kidney Dis VL - 16 IS - 2 N2 - Patients with chronic kidney disease (CKD), especially those requiring maintenance hemodialysis treatments, may lose up to 3 g of iron each year because of frequent blood losses. Higher doses of erythropoiesis-stimulating agents (ESAs) may worsen iron depletion and lead to an increased platelet count (thrombocytosis), ESA hyporesponsiveness, and hemoglobin variability. Hence, ESA therapy requires concurrent iron supplementation. Traditional iron markers such as serum ferritin and transferrin saturation ratio (TSAT) (ie, serum iron divided by total iron-binding capacity [TIBC]), may be confounded by non-iron-related conditions. Whereas serum ferritin <200 ng/mL suggests iron deficiency in CKD patients, ferritin levels between 200 and 1,200 ng/mL may be related to inflammation, latent infections, malignancies, or liver disease. Protein-energy wasting may lower TIBC, leading to a TSAT within the normal range, even when iron deficiency is present. Iron and anemia indices have different mortality predictabilities, in that high serum ferritin but low iron, TIBC, and TSAT levels are associated with increased mortality, whereas hemoglobin exhibits a U-shaped risk for death. The increased mortality associated with targeting hemoglobin above 13 g/dL may result from iron depletion-associated thrombocytosis. Intravenous (IV) iron administration may not only decrease hemoglobin variability and ESA hyporesponsiveness, it may also reduce the greater mortality associated with the much higher ESA doses that have been used in some patients when targeting higher hemoglobin levels. SN - 1548-5609 UR - https://www.unboundmedicine.com/medline/citation/19233073/Intravenous_iron_versus_erythropoiesis_stimulating_agents:_friends_or_foes_in_treating_chronic_kidney_disease_anemia L2 - https://linkinghub.elsevier.com/retrieve/pii/S1548-5595(08)00215-2 DB - PRIME DP - Unbound Medicine ER -