Evaluation Of Statin Anti-Inflammatory Effect On Atherosclerosis In Chronic Kidney Disease

Background and Aim: Cardiovascular mortality in chronic kidney disease patients has been associated with increased markers of inflammation. CD4+CD28 null cells are implicated in inflammation and destabilization of atherosclerotic plaques. It has been shown that statins can inhibit inflammatory markers. We aimed to determine the effect of statin therapy as anti-inflammatory agents on the level of CD4+CD28 null cells over a period of three months. Materials and Methods: This study was conducted on 90 patients, 60 hemodialysis patients (group 1) and 30 patients with chronic kidney disease on conservative treatment (group 2), in addition to 30 control subjects (group 3). All patients and controls were subjected to full history, clinical examination and routine laboratory tests. The micro-inflammatory state was detected by estimation of CRP and TNF alpha. Carotid intima media thickness (CIMT) was studied by carotid duplex and CD4+CD28 null cell expansion was determined by flow cytometric analysis of T cell subsets. All patients received atorvastatin 20 mg per day for a period of three months, after which special laboratory tests were repeated again. Results: The laboratory data showed significant increase in cholesterol, triglycerides, CRP, CD4+CD28 null cells, TNF and CIMT in groups 1 and 2 compared to the control group. Statin use was associated with a significant decrease in CD4+CD28 null cells in both patient groups compared to the control group (P<0.0001), while CIMT was not affected in either group. Conclusion: Statins can be used as anti-inflammatory agents in chronic kidney disease patients leading to a significant decrease in CD4+CD28 null T cell percentage.