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慢性肾脏病中的炎症和恶病质。

Inflammation and cachexia in chronic kidney disease.

机构信息

Division of Pediatrics Nephrology, Department of Pediatrics, University of California San Diego, La Jolla, CA 92093-0634, USA.

出版信息

Pediatr Nephrol. 2010 Apr;25(4):711-24. doi: 10.1007/s00467-009-1427-z. Epub 2010 Jan 29.

Abstract

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-kappaB 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.

摘要

慢性炎症与慢性肾脏病(CKD)和终末期肾病(ESRD)患者的恶病质和死亡风险增加有关。炎症会抑制食欲并导致蛋白质储存流失。在 CKD 患者中,促炎细胞因子血清水平升高可能是由于肾功能降低、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合并症的存在引起的。恶病质是由于食欲急剧下降和脂肪及瘦体重分解代谢增加的协同作用引起的。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-κB 和 ATP-泛素依赖性蛋白水解途径提供信号,导致肌肉消耗。对导致炎症和恶病质的分子途径的进一步研究可能为这种慢性疾病的破坏性和潜在致命并发症提供新的治疗方法。

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