Growth hormone induces anabolism in malnourished maintenance haemodialysis patients

Abstract

Background. Growth hormone (GH) promotes anabolism in patients undergoing maintenance haemodialysis (MHD). However, no studies have examined the effects of GH on protein anabolism in MHD patients using full nitrogen-balance techniques. This study tested the hypothesis that recombinant human GH (rhGH) will induce an anabolic response, as assessed by long-term classic nitrogen-balance techniques, in malnourished MHD patients. Methods. Six adult MHD patients with protein-energy malnutrition underwent nitrogen-balance studies in a general clinical research centre for 28-35 days each. Patients were maintained on a constant dialysis regimen and protein and energy intakes that were similar to their dialysis regimen and diet prior to hospitalization. The first 14-21 hospital days constituted a baseline phase; during the subsequent 8-21 days, patients were given daily subcutaneous injections of rhGH (0.05mg/kg body weight/day). Results. During treatment with rhGH, serum insulin-like growth factor-I (IGF-I) increased by ∼225% (P = 0.002), nitrogen balance became strongly positive (+2.35 g/day; P = 0.034 vs baseline) and there was a reduction in serum urea nitrogen (-32%; P = 0.001). Two patients who became acutely ill and had the lowest dietary protein intakes developed a much smaller rise in serum IGF-I levels and increase in nitrogen balance when they received the rhGH treatment. In the remaining four responders, the decrease in nitrogen output was sustained throughout the entire period of treatment with rhGH. There was no change in body weight during the baseline or treatment phases of the study. Conclusions. Injections of rhGH induce a strong and sustained anabolic effect, as indicated by positive nitrogen balance, in MHD patients with protein-energy malnutrition. This response was attenuated in two patients who were acutely ill with low protein intakes, suggesting that they may have developed partial resistance to GH. © The Author [2005]. Published by Oxford University Press on behalf of ERA-EDTA. All rights reserved.