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T. Bragadesh, S. Bhandari, Deferiprone, iron overload in a renal transplant patient, QJM: An International Journal of Medicine, Volume 107, Issue 6, June 2014, Pages 465–466, https://doi.org/10.1093/qjmed/hct254
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Regular red blood cell transfusion is the mainstay of treatment in patients with symptomatic refractory anaemia. Repeated transfusions result in accumulation of iron in the heart, liver and pancreas which lead to the production of reactive oxygen species, which may lead to cellular dysfunction, and in the longer term to cell necrosis and apoptosis.1 Iron chelation therapy reduces this tissue iron deposition.
Three iron chelating agents are available. Parenteral (intravenous or subcutaneous) deferoxamine reduces myocardial and liver iron concentrations and is excreted mainly by the kidneys.1 Desferrioxamine is associated with acute kidney injury and acute tubular dysfunction (mainly proximal).2 Deferasirox, an oral iron chelator with primarily hepatobillary excretion,1 is as effective in treating iron overload but has been associated with acute kidney injury, an increased incidence of reversible Fanconi syndrome and transient rises in serum creatinine (SC).2 Deferiprone is licensed for the treatment of patients with thalassaemia major when deferoxamine therapy is contraindicated or inadequate and is effective in removing intracellular iron from the heart and other tissues.2 It has been associated with 1–2% agranulosytosis, and potentially increased liver enzymes.3,4 Chelator use has not been described in transplant patients or those with significant renal impairment.
