title: The effect of high-flux hemodialysis on renal anemia.
abstract: BACKGROUND
  Anemia is an important predictor of mortality and morbidity in patients with end-stage renal disease (ESRD) undergoing hemodialysis (HD). Erythropoietin (EPO) is an expensive drug, which increases the cost of therapy. In addition, anemia persists in 20-30% of cases despite EPO treatment. In this study, which depended on the idea that the clearance of moderate and high molecular weight erythropoiesis inhibitors leads to an improvement in terms of anemia, we aimed to investigate the effect of high-flux dialysis on anemia and EPO requirement in patients undergoing HD.
  
  
  METHODS
  The study included 48 patients with ESRD on chronic HD treatment who could not reach the target hemoglobin (Hb) level, despite treatment with at least 200 IU/kg/week subcutaneous EPO. Patients were randomized into two groups and HD was performed with polysulphone low-flux dialyzer (Fresenius F6 HPS) or polysulphone high-flux dialyzer (Fresenius F60) for 6 months.
  
  
  RESULTS
  Although the EPO doses were significantly lower (p<0.001) in the high-flux dialysis group, Hb levels showed a significant increase (p<0.001). In the low-flux dialysis group, Hb levels showed no significant increase, despite the steady increase in EPO doses. In the high-flux group, the reduction of beta2-microglobulin (b2-MG) and phosphorus levels during dialysis was significantly higher when compared to the low-flux group (p<0.001). During the follow-up period, while b2-MG levels decreased significantly in the high-flux group (p<0.05), there was an increase in the low-flux group (p<0.05). Kt/V(urea) values showed no significant difference throughout the study.
  
  
  CONCLUSIONS
  Our results suggest that high-flux dialysis use is effective and this can be an alternative method in terms of controlling renal anemia and reducing the cost of therapy. These beneficial effects of high-flux dialysis are probably mediated by the improved clearance of moderate and high molecular weight toxins.
authors.affiliation: Department of Nephrology, Ankara Numune Education and Research Hospital, Ankara, Turkey.
authors.forename: Deniz
authors.initials: D
authors.lastname: Ayli
authors.forename: Meltem
authors.initials: M
authors.lastname: Ayli
authors.forename: Alper
authors.initials: A
authors.lastname: Azak
authors.forename: Cüneyt
authors.initials: C
authors.lastname: Yüksel
authors.forename: Gözde Petek
authors.initials: GP
authors.lastname: Kosmaz
authors.forename: Gökhan
authors.initials: G
authors.lastname: Atilgan
authors.forename: Fatih
authors.initials: F
authors.lastname: Dede
authors.forename: Ekrem
authors.initials: E
authors.lastname: Abayli
authors.forename: Mine
authors.initials: M
authors.lastname: Camlibel
mesh_terms: D000328:Adult; D000368:Aged; D000369:Aged, 80 and over; D000740:Anemia / Q000097:blood / Q000209:etiology / Q000517:prevention & control*; D004351:Drug Resistance; D004921:Erythropoietin; D005260:Female; D006454:Hemoglobins / Q000378:metabolism; D006801:Humans; D007676:Kidney Failure, Chronic / Q000097:blood / Q000150:complications* / Q000628:therapy*; D008297:Male; D008567:Membranes, Artificial; D008875:Middle Aged; D011994:Recombinant Proteins; D006435:Renal Dialysis / Q000295:instrumentation*
chemical_list: D006454:Hemoglobins; D008567:Membranes, Artificial; D011994:Recombinant Proteins; C103998:epoetin beta; D004921:Erythropoietin