title: Marked reductions in bioactive insulin-like growth factor I (IGF-I) during hemodialysis.
abstract: OBJECTIVE
  Hemodialysis (HD) patients lose lean body mass, even when they are adequately dialysed. One reason may be a decreased activity of the IGF-system. However, data on changes in bioactive IGF-I during HD are sparse.
  
  
  METHODS
  Ten stable, non-diabetic HD patients were studied with 30 min intervals during a scheduled HD, with blood sampling before (-15 and 0 min), during (4 h) and after (1 h) the session. Patients were fasted for at least 6 h before and during the study. Arterial and venous blood was sampled for determination of IGF-I bioactivity, free and total IGF-I and IGF-II, IGF binding protein-1 (IGFBP-1), IGFBP-1 complexed IGF-I and IGFBP-2.
  
  
  RESULTS
  Total IGF-I and -II decreased marginally (<12%) at the very end of the study (P<0.05). By contrast, at 3 h free and bioactive IGF-I had declined by approximately 35% and 50%, respectively, and levels remained suppressed for the rest of the study (P<0.05). Concomitantly, IGFBP-1 and IGFBP-1:IGF-I complex formation increased 5.0-fold and 2.6-fold, respectively (P<0.05). By contrast, IGFBP-2 did not increase as a result of HD. No major differences between arterial and venous concentrations were observed.
  
  
  CONCLUSIONS
  Despite marginal reductions in total IGF-I and -II, bioactive and free IGF-I declined markedly during and after HD. This is likely a consequence of the increase in IGFBP-1, sequestering free IGF-I, and reducing bioactive IGF-I. Based on the present data we hypothesize that the catabolism induced by HD is in part related to the observed reductions in bioactive IGF-I.
authors.affiliation: Department of Renal Medicine C, Aarhus University Hospital, Skejby Sygehus, Aarhus N, Denmark. pi@dadlnet.dk
authors.forename: Per
authors.initials: P
authors.lastname: Ivarsen
authors.forename: Jian-Wen
authors.initials: JW
authors.lastname: Chen
authors.forename: Ida
authors.initials: I
authors.lastname: Tietze
authors.forename: Jens Sandahl
authors.initials: JS
authors.lastname: Christiansen
authors.forename: Allan
authors.initials: A
authors.lastname: Flyvbjerg
authors.forename: Jan
authors.initials: J
authors.lastname: Frystyk
mesh_terms: D000328:Adult; D000368:Aged; D002478:Cells, Cultured; D015536:Down-Regulation; D005260:Female; D019382:Human Growth Hormone / Q000032:analysis / Q000097:blood; D006801:Humans; D007118:Immunoassay; D007328:Insulin / Q000032:analysis / Q000097:blood; D018969:Insulin-Like Growth Factor Binding Proteins / Q000032:analysis / Q000097:blood; D007334:Insulin-Like Growth Factor I / Q000032:analysis / Q000378:metabolism*; D007676:Kidney Failure, Chronic / Q000097:blood* / Q000378:metabolism / Q000628:therapy*; D008297:Male; D008875:Middle Aged; D006435:Renal Dialysis; D013997:Time Factors; D055815:Young Adult
chemical_list: D007328:Insulin; D018969:Insulin-Like Growth Factor Binding Proteins; D019382:Human Growth Hormone; D007334:Insulin-Like Growth Factor I