Inflammation and cachexia in chronic kidney disease
Inflammation and cachexia in chronic kidney disease
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DOI：
10.1007/s00467-009-1427-z
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发表时间：
2010-04-01
影响因子：
3
通讯作者：
Mak, Robert H.
中科院分区：
文献类型：
--
作者：
Cheung, Wai W.;Paik, Kyung Hoon;Mak, Robert H.
慢性炎症与慢性肾病（CKD）和终末期肾病（ESRD）患者的恶病质和死亡风险增加相关。炎症抑制食欲，导致蛋白质储存的损失。在CKD患者中，促炎性细胞因子的血清水平升高可能由肾功能降低、容量超负荷、氧化或羰基应激、抗氧化剂水平降低、尿毒症感染易感性增加以及存在共病引起。恶病质是由食欲急剧下降和脂肪和瘦体重增加的协同组合引起的。促炎细胞因子作用于中枢神经系统，改变食欲和能量代谢，并通过核因子-κ B和ATP-泛素依赖性蛋白水解途径提供信号，导致肌肉萎缩。对导致炎症和恶病质的分子途径的进一步研究可能会为这种破坏性和潜在致命的慢性疾病并发症带来新的治疗方法。
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.