Plasma sTWEAK and PTX3: New Determinant Tools of Cardiovascular Outcome Also in Patients with CKD

[摘要] Chronic kidney disease (CKD) is strongly associated with cardiovascular disease (CVD), which may account for 50% of all death (1). Irrespective of the cause of renal disease, there is firm evidence that a chronic proinflammatory state and progressive atherosclerosis coexist in patients with CKD and that inflammation contributes to cardiovascular morbidity and mortality (2,3). This inflammatory phenomenon is frequently observed even before the beginning of chronic renal replacement therapy. Consequently, a distinction must be made between the contributions of general risk factors to the development of CVD, risk factors related to CKD, and risk factors specifically related to chronic dialysis. Thus, the link between atherosclerosis and increased CVD risk in patients with CKD has been difficult to define, mainly because of the coexistence of several cardiovascular risk factors in this population, including increased oxidative stress, microinflammation, physical inactivity, anemia, vascular calcification, endothelial dysfunction, and reduced nitric oxide availability. Whether as primary or secondary mediators, serum proinflammatory cytokine levels are significantly associated with this increased risk for mortality (4). As atherosclerosis is clearly accepted as an inflammatory state characterized by infiltration of lipid-laden macrophages into the vascular wall, the complex interaction of inflammatory cells with the normal residents of the vascular wall (i.e., endothelial and smooth muscle cells) directs the progression of the disease (5). Inflammatory cells secrete a variety of chemokines and cytokines that have a profound effect on the development and progression of the plaque. Moreover, many of these cytokines can mediate both pro- and antiatherogenic processes depending on the cellular milieu.

[学科分类] 泌尿医学

[关键词] Bone marrow necrosis;Sickle cell disease;Hyperhemolysis syndrome