title: Hemodialysis-associated hemosiderosis in the era of erythropoiesis-stimulating agents: a MRI study.
abstract: BACKGROUND
  Most dialysis patients receiving erythropoesis-stimulating agents (ESA) also receive parenteral iron supplementation. There are few data on the risk of hemosiderosis in this setting.
  
  
  METHODS
  We prospectively measured liver iron concentration by means of T1 and T2* contrast magnetic resonance imaging (MRI) without gadolinium, in a cohort of 119 fit hemodialysis patients receiving both parenteral iron and ESA, in keeping with current guidelines.
  
  
  RESULTS
  Mild to severe hepatic iron overload was observed in 100 patients (84%; confidence interval, [CI] 76%-90%), of whom 36% (CI, 27%-46%) had severe hepatic iron overload (liver iron concentration >201 μmol/g of dry weight). In the cross-sectional study, infused iron, hepcidin, and C-reactive protein values correlated with hepatic iron stores in both univariate analysis (P<.05, Spearman test) and binary logistic regression (P <.05). In 11 patients who were monitored closely during parenteral iron therapy, the iron dose infused per month correlated strongly with both the overall increase and the monthly increase in liver iron concentration (respectively, rho=0.66, P=.0306 and rho=0.85, P=0.0015, Spearman test). In the 33 patients with iron overload, iron stores fell significantly after iron withdrawal or after a major reduction in the iron dose (first MRI: 220 μmol/g (range: 60-340); last MRI: 50 μmol/g (range: 5-210); P <.0001, Wilcoxon's paired test).
  
  
  CONCLUSIONS
  Most hemodialysis patients receiving ESA and intravenous iron supplementation have hepatic iron overload on MRI. These findings call for a revision of guidelines on iron therapy in this setting, especially regarding the amount of iron infused and noninvasive methods for monitoring iron stores.
authors.affiliation: Division of Nephrology and Dialysis, Hôpital Privé Claude Galien, Générale de Santé, Quincy Sous Sénart, France. rostotom@orange.fr
authors.forename: Guy
authors.initials: G
authors.lastname: Rostoker
authors.forename: Mireille
authors.initials: M
authors.lastname: Griuncelli
authors.forename: Christelle
authors.initials: C
authors.lastname: Loridon
authors.forename: Renaud
authors.initials: R
authors.lastname: Couprie
authors.forename: Abbes
authors.initials: A
authors.lastname: Benmaadi
authors.forename: Catherine
authors.initials: C
authors.lastname: Bounhiol
authors.forename: Myriam
authors.initials: M
authors.lastname: Roy
authors.forename: Gabrielle
authors.initials: G
authors.lastname: Machado
authors.forename: Phillippe
authors.initials: P
authors.lastname: Janklewicz
authors.forename: Gilles
authors.initials: G
authors.lastname: Drahi
authors.forename: Hervé
authors.initials: H
authors.lastname: Dahan
authors.forename: Yves
authors.initials: Y
authors.lastname: Cohen
mesh_terms: D000328:Adult; D000368:Aged; D000369:Aged, 80 and over; D000740:Anemia / Q000188:drug therapy* / Q000209:etiology; D015415:Biomarkers / Q000378:metabolism; D003430:Cross-Sectional Studies; D004359:Drug Therapy, Combination; D005260:Female; D005290:Ferric Compounds / Q000009:adverse effects* / Q000627:therapeutic use; D000077605:Ferric Oxide, Saccharated; D005937:Glucaric Acid / Q000009:adverse effects* / Q000627:therapeutic use; D006397:Hematinics / Q000009:adverse effects* / Q000627:therapeutic use; D006486:Hemosiderosis / Q000139:chemically induced* / Q000175:diagnosis / Q000378:metabolism; D006801:Humans; D007262:Infusions, Intravenous; D007501:Iron / Q000378:metabolism; D007676:Kidney Failure, Chronic / Q000150:complications / Q000628:therapy*; D008099:Liver / Q000378:metabolism; D016015:Logistic Models; D008137:Longitudinal Studies; D008279:Magnetic Resonance Imaging; D008297:Male; D008875:Middle Aged; D011446:Prospective Studies; D006435:Renal Dialysis / Q000009:adverse effects
chemical_list: D015415:Biomarkers; D005290:Ferric Compounds; D006397:Hematinics; D007501:Iron; D000077605:Ferric Oxide, Saccharated; D005937:Glucaric Acid