Inflammation and cachexia in chronic kidney disease

被引:135
作者
Cheung, Wai W. [1 ]
Paik, Kyung Hoon [2 ]
Mak, Robert H. [1 ]
机构
[1] Univ Calif San Diego, Dept Pediat, Div Pediat Nephrol, La Jolla, CA 92093 USA
[2] Sungkyunkwan Univ, Sch Med, Samsung Med Ctr, Dept Pediat, Seoul, South Korea
关键词
Cachexia; Chronic kidney disease; Cytokines; End-stage renal failure; Inflammation; Melanocortin signaling; Muscle wasting; Neuropeptides; C-REACTIVE PROTEIN; STAGE RENAL-DISEASE; NF-KAPPA-B; MELANOCORTIN-4 RECEPTOR ANTAGONIST; LEFT-VENTRICULAR HYPERTROPHY; PERITONEAL-DIALYSIS PATIENTS; FOXO TRANSCRIPTION FACTORS; UREMIA-ASSOCIATED CACHEXIA; SKELETAL-MUSCLE ATROPHY; CORONARY-HEART-DISEASE;
D O I
10.1007/s00467-009-1427-z
中图分类号
R72 [儿科学];
学科分类号
100202 ;
摘要
Chronic inflammation is associated with cachexia and increased mortality risk in patients with chronic kidney disease (CKD) and end-stage renal disease (ESRD). Inflammation suppresses appetite and causes the loss of protein stores. In CKD patients, increased serum levels of pro-inflammatory cytokines may be caused by reduced renal function, volume overload, oxidative or carbonyl stress, decreased levels of antioxidants, increased susceptibility to infection in uremia, and the presence of comorbid conditions. Cachexia is brought about by the synergistic combination of a dramatic decrease in appetite and an increase in the catabolism of fat and lean body mass. Pro-inflammatory cytokines act on the central nervous system to alter appetite and energy metabolism and to provide a signal-through the nuclear factor-kappa B and ATP-ubiquitin-dependent proteolytic pathways-that causes muscle wasting. Further research into the molecular pathways leading to inflammation and cachexia may lead to novel therapeutic therapies for this devastating and potentially fatal complication of chronic disease.
引用
收藏
页码:711 / 724
页数:14
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