Abstract
Iron overload was a common problem in patients with chronic kidney disease (CKD) treated with dialysis before the availability of recombinant human erythropoietin (rHuEPO). Iron overload during that time was mainly due to a combination of a hypoproliferative erythroid bone marrow along with frequent administration of packed red blood cell (PRBC) transfusions to manage symptomatic anemia [1]. The result of iron overload was hepatomegaly, hypersplenism and hyperpigmentation. Cirrhosis could also develop as a result of transfusion-related hepatitis infection. Intravenous (IV) iron has also been reported to cause iron overload in patients concomitantly receiving PRBCs in the pre-rHuEPO era [1]. The use of IV iron with or without concomitant PRBCs also contributed to iron overloading in the past and was associated with iron deposits in liver reticuloendothelial and parenchymal cells. However, iron overloading was not associated with functional changes in the liver (i.e., increases in liver function tests or cirrhosis) unless PRBC transfusions resulted in viral hepatitis [1].
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St. Peter, W.L. (2002). Is long-term intravenous iron therapy risky?. In: Ifudu, O. (eds) Renal Anemia. Springer, Dordrecht. https://doi.org/10.1007/978-94-015-9998-6_12
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DOI: https://doi.org/10.1007/978-94-015-9998-6_12
Publisher Name: Springer, Dordrecht
Print ISBN: 978-90-481-6045-7
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