Department of Education and Research, Hospital Eugenio Espejo, Quito, Ecuador.
Division of Renal Medicine and Baxter Novum, Karolinska Institutet, Stockholm, Sweden.
Nephrol Dial Transplant. 2018 Oct 1;33(suppl_3):iii35-iii40. doi: 10.1093/ndt/gfy175.
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.
在正常情况下，炎症是对各种有害刺激的一种保护和生理反应。然而，在一些慢性衰弱性疾病中，如慢性肾脏病，炎症变得适应不良、失控和持续存在。全身持续炎症近 20 年来一直被认为是导致尿毒症表型（如心血管疾病、蛋白质能量消耗、抑郁、骨质疏松和虚弱）的主要因素，也是心血管和总死亡率的预测因素。由于炎症在机制上与多种衰老过程（炎性衰老）有关，因此它可能是尿毒症环境中导致早衰表型的主要因素。炎症可能是多因素病因的结果，并与尿毒症毒素积聚时出现的许多因素相互作用。除了旨在减少尿毒症环境中炎症分子产生的干预措施外，增加清除大中分子的新策略，如扩展血液透析，可能是减少与保留中分子量尿毒症毒素相关的炎症适应负荷的机会。
