title: Immune mechanisms involved in cardiovascular complications of chronic kidney disease.
abstract: A sustained status of chronic inflammation is closely linked to several complications of chronic kidney disease (CKD), such as vascular degeneration, myocardial fibrosis, loss of appetite, insulin resistance, increased muscle catabolism and anemia. These consequences of a chronically activated immune system impact on the acceleration of atherosclerosis, vascular calcification and development of heart dysfunction. Recent evidence suggests that these immune-mediated consequences of uremic toxicity are not only important to stratify the risk and understand the mechanisms of disease, but also represent an important area for intervention. Thus, the aim of this brief review is to discuss the immune mechanisms behind atherosclerosis and myocardiopathy in CKD. We also display the emerging evidence that strategies focusing on modulating the immune response or reducing the generation of triggers of inflammation may represent an important tool to reduce mortality in this group of patients. Ongoing studies may generate the evidence that will translate these strategies to definitive changes in clinical practice.
authors.affiliation: Center for Health and Biological Sciences, Pontifícia Universidade Católica do Paraná, Curitiba, Brazil.
authors.forename: Andréa E M
authors.initials: AE
authors.lastname: Stinghen
authors.forename: Sergio
authors.initials: S
authors.lastname: Bucharles
authors.forename: Miguel C
authors.initials: MC
authors.lastname: Riella
authors.forename: R
authors.initials: R
authors.lastname: Pecoits-Filho
mesh_terms: D047228:Angiotensin II Type 1 Receptor Blockers / Q000627:therapeutic use; D000806:Angiotensin-Converting Enzyme Inhibitors / Q000627:therapeutic use; D000818:Animals; D000893:Anti-Inflammatory Agents / Q000627:therapeutic use; D000959:Antihypertensive Agents / Q000627:therapeutic use; D000975:Antioxidants / Q000627:therapeutic use; D050197:Atherosclerosis / Q000209:etiology / Q000276:immunology / Q000517:prevention & control; D009202:Cardiomyopathies / Q000209:etiology / Q000276:immunology / Q000517:prevention & control; D002318:Cardiovascular Diseases / Q000209:etiology* / Q000276:immunology / Q000517:prevention & control; D002908:Chronic Disease; D002986:Clinical Trials as Topic; D004730:Endothelium, Vascular / Q000503:physiopathology; D006801:Humans; D019161:Hydroxymethylglutaryl-CoA Reductase Inhibitors / Q000627:therapeutic use; D007249:Inflammation / Q000188:drug therapy / Q000209:etiology / Q000276:immunology; D015850:Interleukin-6 / Q000378:metabolism; D007674:Kidney Diseases / Q000150:complications* / Q000276:immunology / Q000628:therapy; D008567:Membranes, Artificial; D051379:Mice; D010518:Periodontitis / Q000150:complications; D006435:Renal Dialysis / Q000009:adverse effects; D014409:Tumor Necrosis Factor-alpha / Q000378:metabolism; D014657:Vasculitis / Q000209:etiology / Q000276:immunology / Q000503:physiopathology
chemical_list: D047228:Angiotensin II Type 1 Receptor Blockers; D000806:Angiotensin-Converting Enzyme Inhibitors; D000893:Anti-Inflammatory Agents; D000959:Antihypertensive Agents; D000975:Antioxidants; D019161:Hydroxymethylglutaryl-CoA Reductase Inhibitors; C508600:IL6 protein, human; D015850:Interleukin-6; D008567:Membranes, Artificial; D014409:Tumor Necrosis Factor-alpha