الفهرس 
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Abstract
Chronic kidney disease (CKD) is associated with a sharp increase in the risk for cardiovascular diseases, which can only be partially explained by known classical risk factors. However, there is a well-established association with increased systemic inflammation. In the last decade, a unique cytotoxic CD4+T cell population has been identified, which can be recognized by the loss of the costimulatory cell surface marker CD28, hence their name CD4+ CD28null T cells. These cells are highly proinflammatory, have the functional features of professional killer lymphocytes and can expand from less than 1% to over 50% of the total CD4+T cell population. In this thesis we show that these cells probably play an important role in destabilizing atherosclerotic plaques and could explain, at least in part, the association of cardiovascular disease with an increased inflammatory milieu in CKD patients.
Within the last decade, expansion of circulating proinflammatory, cytotoxic CD4+CD28null T cells has been identified as a novel nontraditional risk factor for cardiovascular disease. Particularly, patients with underlying conditions that are associated with an activated and dysregulated T cell system, such as ESRD, are prone to expansion of these cells.
CD4+T cell subsets lacking surface CD28 in peripheral blood have been suggested to predispose people to atherosclerosis. So we aimed to determine if CD4+CD28 null T cells are involved in the immune pathological process of atherosclerotic damage in CKD patients
Summary
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predialysis and end-stage renal disease (ESRD) patients undergoing hemodialysis (HD).