Persistent Inflammation as a Catalyst for Other Risk Factors in Chronic Kidney Disease: A Hypothesis Proposal
Persistent Inflammation as a Catalyst for Other Risk Factors in Chronic Kidney Disease: A Hypothesis Proposal
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DOI：
10.2215/cjn.02720409
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发表时间：
2009-12-01
影响因子：
9.8
通讯作者：
Stenvinkel, Peter
中科院分区：
文献类型：
--
作者：
Carrero, Juan Jesus;Stenvinkel, Peter
由于炎症现在是一个“传统”的发现，预测预后不良和心血管事件在绝大多数患者与终末期肾病，它可以说，炎症生物标志物不应该再被认为是“新的”危险因素。在这篇综述中，我们提出的假设，除了推定的直接致动脉粥样硬化的影响，持续的炎症可能作为一种催化剂，并在毒性尿毒症环境中，调节其他并发血管和营养风险因素的影响。我们讨论了最近的一些观察性研究，表明持续性炎症的存在通过与炎症级联反应的自我增强以及消瘦和血管钙化过程的恶化相关的机制放大了不良结局的风险。由于持续性炎症可能是慢性肾脏疾病中其他常见病理生理学改变的沉默罪魁祸首，因此必须定期监测炎症标志物，并尝试针对该患者组中持续性低度炎症进行治疗。Clin J Ain Soc Nephrol 4：S49-S55，2009。doi：10.2215/CJN.02720409
Because inflammation by now is a "traditional" finding that predicts poor outcome and cardiovascular events in the vast majority of patients with ESRD, it could be argued that inflammatory biomarkers should not longer be considered "novel" risk factors. In this review, we forward the hypothesis that, in addition to putative direct proatherogenic effects, persistent inflammation may serve as a catalyst and, in the toxic uremic milieu, modulate the effects of other concurrent vascular and nutritional risk factors. We discuss some recent observational studies, suggesting that the presence of persistent inflammation magnifies the risk for poor outcome via mechanisms related to self-enhancement of the inflammatory cascade and exacerbation of both the wasting and the vascular calcification processes. Because persistent inflammation may be the silent culprit of other commonly observed pathophysiologic alterations in chronic kidney disease, it is imperative that inflammatory markers be regularly monitored and therapeutic attempts be made to target persistent low-grade inflammation in this patient group. Clin J Ain Soc Nephrol 4: S49-S55, 2009. doi: 10.2215/CJN.02720409