title: Growth hormone treatment in hemodialysis patients--a randomized, double-blind, placebo-controlled study.
abstract: OBJECTIVE
  Renal failure and hemodialysis (HD) affect the anabolic growth hormone (GH)-insulin-like growth factor (IGF) axis. A positive correlation between serum IGF-I and normalized protein catabolic rate (PCRn) in HD patients has been reported, and the aim of this study was to assess the metabolic impact of recombinant human (rh)GH in these patients.
  
  
  METHODS
  In a randomized, double-blind, placebo-controlled study, rhGH was given to 35 HD patients for 8 weeks: 0.025 IU/kg/day for 1 week, increasing to 0.05 IU/kg/day. Patients with diabetes, malignancy or clinical signs of infection and those receiving steroid treatment were excluded.
  
  
  RESULTS
  All patients completed the study. Side-effects were rare and equally distributed between the two groups. Post-treatment, serum IGF-I and IGF-I standard deviation score (IGF-I SD) increased in the rhGH group compared to the placebo group: 283+/-33 vs 151+/-16 mg/l (p = 0.001) and 1.8+/-0.6 vs -0.2+/-0.6 (p = 0.002), respectively. IGF binding protein-3 was higher in the rhGH group compared to the placebo group: 5859+/-285 vs 4369+/-321 mg/l (p = 0.002). PCRn was significantly higher in the rhGH group compared to the placebo group: 1.09+/-0.06 vs 0.90+/-0.06 g/kg/day (p = 0.029). No differences were found in body weight, serum albumin or leptin between the two groups. There was no change in C-reactive protein (CRP) in the rhGH group compared to the placebo group: 17.4+/-9.0 vs 12.3+/-4.6 mg/l (p = NS). When the patients were subgrouped according to the CRP level (< or > 10 mg/1), the effect on PCRn persisted only in rhGH-treated subjects with a normal CRP level: 1.10+/-0.08 vs 0.81+/-0.09 g/kg/day (p = 0.025).
  
  
  CONCLUSIONS
  Treatment of HD patients with rhGH at a moderate dose causes augmentation of PCRn which is considered to indicate a higher dietary protein intake. The anabolic effect of rhGH seems to be abolished by subclinical inflammation.
authors.affiliation: Department of Nephrology, Karolinska Hospital, Stockholm, Sweden.
authors.forename: Folke
authors.initials: F
authors.lastname: Ericsson
authors.forename: José C Divino
authors.initials: JC
authors.lastname: Filho
authors.forename: Björn F
authors.initials: BF
authors.lastname: Lindgren
mesh_terms: D000328:Adult; D000368:Aged; D015992:Body Mass Index; D002097:C-Reactive Protein / Q000032:analysis / Q000187:drug effects; D004305:Dose-Response Relationship, Drug; D004311:Double-Blind Method; D004334:Drug Administration Schedule; D004734:Energy Metabolism / Q000187:drug effects*; D005260:Female; D005500:Follow-Up Studies; D019382:Human Growth Hormone / Q000627:therapeutic use*; D006801:Humans; D018836:Inflammation Mediators / Q000032:analysis*; D007676:Kidney Failure, Chronic / Q000175:diagnosis / Q000188:drug therapy* / Q000628:therapy; D007677:Kidney Function Tests; D008297:Male; D008875:Middle Aged; D011336:Probability; D012016:Reference Values; D006435:Renal Dialysis / Q000379:methods*; D018570:Risk Assessment; D016019:Survival Analysis; D016896:Treatment Outcome
chemical_list: D018836:Inflammation Mediators; D019382:Human Growth Hormone; D002097:C-Reactive Protein