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Chronic inflammation in end-stage renal disease and dialysis

期刊

NEPHROLOGY DIALYSIS TRANSPLANTATION
卷 33, 期 -, 页码 35-40

出版社

OXFORD UNIV PRESS
DOI: 10.1093/ndt/gfy175

关键词

chronic inflammation; end stage renal disease; expanded hemodialyisis; middle molecules

资金

  1. Baxter Healthcare Corporation
  2. Heart and Lung Foundation
  3. Stockholm County Council (ALF)

向作者/读者索取更多资源

Under normal conditions, inflammation is a protective and physiological response to various harmful stimuli. However, in several chronic debilitating disorders, such as chronic kidney disease, inflammation becomes maladaptive, uncontrolled and persistent. Systemic persistent inflammation has, for almost 20 years, been recognized as a major contributor to the uraemic phenotype (such as cardiovascular disease, protein energy wasting, depression, osteoporosis and frailty), and a predictor of cardiovascular and total mortality. Since inflammation is mechanistically related to several ageing processes (inflammageing), it may be a major driver of a progeric phenotype in the uraemic milieu. Inflammation is likely the consequence of a multifactorial aetiology and interacts with a number of factors that emerge when uraemic toxins accumulate. Beside interventions aiming to decrease the production of inflammatory molecules in the uraemic milieu, novel strategies to increase the removal of large middle molecules, such as expanded haemodialysis, may be an opportunity to decrease the inflammatory allostatic load associated with retention of middle molecular weight uraemic toxins.

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