title: Characterization of hepatic and cardiac iron deposition during standard treatment of anaemia in haemodialysis.
abstract: BACKGROUND
  Parenteral iron is integral in the treatment of anaemia of chronic kidney disease patients on haemodialysis (HD). However, increased liver iron concentration (LIC) can result from such treatment, and this correlates poorly with serum ferritin or transferrin saturation values. It is unclear whether increased cardiac iron concentration also occurs in this setting. We aimed to evaluate the relationship of intravenous iron supplementation to hepatic and cardiac iron deposition in chronic HD subjects.
  
  
  METHODS
  A cohort of 10 patients on chronic HD for at least 1 year underwent MRI-based quantitation of hepatic and cardiac iron content to evaluate the relationship between intravenous iron supplements and hepatic and cardiac iron deposition. The results were compared against the cumulative parenteral iron dose and serum iron markers.
  
  
  RESULTS
  The median age was 61 years (95% confidence interval (CI) 50-71), HD time 2.5 years (95%CI 2.0-5.3) and cumulative iron dose 4300 mg (95%CI 2110-9045). Hepatic iron concentration was elevated in eight of 10 subjects (median 46 mmol/kg, range 31-76). Cardiac iron levels were within the reference range in all subjects. There was poor correlation between conventional haematinic values and either LIC or cardiac iron levels. None of the study subjects exhibited elevated cardiac iron concentration.
  
  
  CONCLUSIONS
  Whilst HD patients receiving standard parenteral iron therapy have elevated LICs, this is not associated with cardiac iron deposition. Transferrin saturation and serum ferritin levels are poor markers of either liver or cardiac iron deposition in HD subjects.
authors.affiliation: Department of Gastroenterology and Hepatology, Fiona Stanley Hospital, Murdoch, Western Australia, Australia.
authors.forename: Richard
authors.initials: R
authors.lastname: Holman
authors.affiliation: Department of Gastroenterology and Hepatology, Fiona Stanley Hospital, Murdoch, Western Australia, Australia.|School of Veterinary and Life Sciences, Murdoch University, Murdoch and School of Biomedical Sciences, Bentley, Western Australia.|Curtin Health Innovation Research Institute, Curtin University, Bentley, Western Australia.
authors.forename: John K
authors.initials: JK
authors.lastname: Olynyk
authors.affiliation: Department of Nephrology, Fremantle Hospital, Perth, Western Australia.
authors.forename: Hemant
authors.initials: H
authors.lastname: Kulkarni
authors.affiliation: Department of Nephrology and Transplantation, Prince of Wales Hospital, Sydney, New South Wales, Australia.|Clinical School, University of New South Wales, Sydney, New South Wales, Australia.
authors.forename: Paolo
authors.initials: P
authors.lastname: Ferrari
mesh_terms: D061605:Administration, Intravenous; D000368:Aged; D000740:Anemia / Q000097:blood / Q000175:diagnosis / Q000188:drug therapy* / Q000209:etiology; D015415:Biomarkers / Q000097:blood; D005260:Female; D005290:Ferric Compounds / Q000008:administration & dosage* / Q000009:adverse effects / Q000378:metabolism; D005293:Ferritins / Q000097:blood; D006397:Hematinics / Q000008:administration & dosage* / Q000009:adverse effects / Q000378:metabolism; D006801:Humans; D008099:Liver / Q000378:metabolism*; D008279:Magnetic Resonance Imaging; D008297:Male; D008875:Middle Aged; D009206:Myocardium / Q000378:metabolism*; D010865:Pilot Projects; D006435:Renal Dialysis / Q000009:adverse effects*; D051436:Renal Insufficiency, Chronic / Q000097:blood / Q000150:complications / Q000175:diagnosis / Q000628:therapy*; D013997:Time Factors; D014018:Tissue Distribution; D014168:Transferrin / Q000378:metabolism; D016896:Treatment Outcome
chemical_list: D015415:Biomarkers; D005290:Ferric Compounds; D006397:Hematinics; D014168:Transferrin; D005293:Ferritins; C013276:teferrol
keywords: MRI; chronic kidney disease; ferritin; heart; iron; liver