title: Relationship between erythropoietin responsiveness, insulin resistance, and malnutrition-inflammation-atherosclerosis (MIA) syndrome in hemodialysis patients with diabetes.
abstract: BACKGROUND
  This study aimed to explore the relationship between recombinant human erythropoietin (EPO) responsiveness, insulin resistance, and malnutrition-inflammation-atherosclerosis (MIA) syndrome in hemodialysis patients.
  
  
  METHODS
  This was an observational cohort study in hemodialysis patients. Adipokines, inflammatory cytokines, and required EPO dosage were measured in diabetes (DM; n=58) and non-diabetes (non-DM; n=58) groups over 48 weeks. Furthermore, the EPO responsiveness index (required EPO dosage divided by hemoglobin) was evaluated with or without MIA syndrome in both groups.
  
  
  RESULTS
  The DM group had significantly higher plasma leptin, interleukin-6 (IL-6), and high sensitivity C-reactive protein (hs-CRP) levels but lower plasma high molecular weight (HMW) adiponectin levels compared to the non-DM group. Although hemoglobin levels were not significantly different, required EPO dosage was significantly higher in the DM group than in the non-DM group, particularly in the presence of MIA syndrome. The DM group with MIA syndrome had significantly higher plasma leptin, IL-6, and hs-CRP levels but lower plasma HMW adiponectin levels compared to the non-DM group with MIA syndrome. There was also a significant association between EPO dosage and homeostasis model assessment for insulin resistance (HOMA-IR), hs-CRP, IL-6, tumor necrosis factor a, leptin, and HMW adiponectin levels in DM patients with MIA syndrome.
  
  
  CONCLUSIONS
  Diabetic hemodialysis patients with MIA syndrome have a lower response to EPO and a higher resistance to insulin. This fact may explain the poor outcome of these patients and demonstrate the importance of diagnosis and therapeutic management.
authors.affiliation: Division of Nephrology, Hypertension and Endocrinology, Department of Internal Medicine, Nihon University School of Medicine, Tokyo - Japan. abe.masanori@nihon-u.ac.jp
authors.forename: Masanori
authors.initials: M
authors.lastname: Abe
authors.forename: Kazuyoshi
authors.initials: K
authors.lastname: Okada
authors.forename: Takashi
authors.initials: T
authors.lastname: Maruyama
authors.forename: Noriaki
authors.initials: N
authors.lastname: Maruyama
authors.forename: Koichi
authors.initials: K
authors.lastname: Matsumoto
authors.forename: Masayoshi
authors.initials: M
authors.lastname: Soma
mesh_terms: D000368:Aged; D000704:Analysis of Variance; D000740:Anemia / Q000097:blood / Q000188:drug therapy* / Q000209:etiology; D050197:Atherosclerosis / Q000097:blood / Q000209:etiology* / Q000503:physiopathology; D015415:Biomarkers / Q000097:blood; D001786:Blood Glucose / Q000378:metabolism; D003924:Diabetes Mellitus, Type 2 / Q000097:blood / Q000150:complications* / Q000503:physiopathology; D004921:Erythropoietin / Q000627:therapeutic use*; D005260:Female; D006442:Glycated Hemoglobin / Q000378:metabolism; D006397:Hematinics / Q000627:therapeutic use*; D006801:Humans; D007249:Inflammation / Q000097:blood / Q000209:etiology* / Q000503:physiopathology; D018836:Inflammation Mediators / Q000097:blood; D007333:Insulin Resistance; D007564:Japan; D007676:Kidney Failure, Chronic / Q000097:blood / Q000150:complications / Q000503:physiopathology / Q000628:therapy*; D008055:Lipids / Q000097:blood; D008297:Male; D044342:Malnutrition / Q000097:blood / Q000209:etiology* / Q000503:physiopathology; D008875:Middle Aged; D011446:Prospective Studies; D011994:Recombinant Proteins; D006435:Renal Dialysis / Q000009:adverse effects*; D013577:Syndrome; D013997:Time Factors; D016896:Treatment Outcome
chemical_list: D015415:Biomarkers; D001786:Blood Glucose; D004921:Erythropoietin; D006442:Glycated Hemoglobin; D006397:Hematinics; D018836:Inflammation Mediators; D008055:Lipids; D011994:Recombinant Proteins; C517652:hemoglobin A1c protein, human