Current opinion in nephrology and hypertension · 2008
Hypercatabolism in dialysis patients.
СтатьяПоддержка NIH: внешняя программаПоддержка исследования: вне правительства СШАОбзорНазвание и аннотация: Перевод пока не подготовлен
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Raj Dominic S C, Sun Yijuan, Tzamaloukas Antonios H
Аннотация
PURPOSE OF REVIEW: This article will provide a comprehensive review and update on recent advances in the field of protein-energy wasting and protein kinetics in patients with end-stage renal disease.
RECENT FINDINGS: Hypercatabolism in dialysis patients is related to intradialytic loss of amino acids as well as cytokine activation. Interleukin-6 pays a central role in regulating whole-body, muscle and hepatic protein turnover during hemodialysis. Amino acids released from the muscle protein catabolism are taken up by the liver for de-novo protein synthesis during hemodialysis. Intradialytic nutrient supplementation increases protein synthesis, but does not attenuate muscle protein catabolism.
SUMMARY: Protein-energy wasting observed in end-stage renal disease is a maladaptive metabolic state, which often coexists with inflammation. Cytokine-adipokine signaling plays an important role in protein-energy wasting. Peripheral blood mononuclear cells and skeletal muscle are important sources of interleukin-6 during hemodialysis. In addition to contributing to intradialytic protein catabolism, interleukin-6 impairs effective utilization of amino acids for protein synthesis. Although muscle protein breakdown increases during hemodialysis, whole-body proteolysis is not increased. The dissociation between regional and whole-body protein kinetics in end-stage renal disease is due to somatic-hepatic recycling of amino acids. Net anabolism during hemodialysis may be achieved only by providing nutrients as well as inhibiting overt inflammatory signals.
RECENT FINDINGS: Hypercatabolism in dialysis patients is related to intradialytic loss of amino acids as well as cytokine activation. Interleukin-6 pays a central role in regulating whole-body, muscle and hepatic protein turnover during hemodialysis. Amino acids released from the muscle protein catabolism are taken up by the liver for de-novo protein synthesis during hemodialysis. Intradialytic nutrient supplementation increases protein synthesis, but does not attenuate muscle protein catabolism.
SUMMARY: Protein-energy wasting observed in end-stage renal disease is a maladaptive metabolic state, which often coexists with inflammation. Cytokine-adipokine signaling plays an important role in protein-energy wasting. Peripheral blood mononuclear cells and skeletal muscle are important sources of interleukin-6 during hemodialysis. In addition to contributing to intradialytic protein catabolism, interleukin-6 impairs effective utilization of amino acids for protein synthesis. Although muscle protein breakdown increases during hemodialysis, whole-body proteolysis is not increased. The dissociation between regional and whole-body protein kinetics in end-stage renal disease is due to somatic-hepatic recycling of amino acids. Net anabolism during hemodialysis may be achieved only by providing nutrients as well as inhibiting overt inflammatory signals.