Objectives Chronic kidney disease and atherosclerosis are considered to be inflammatory process in which T cells and cytokines participate. This study determines the effect of statin therapy as an anti-inflammatory agent on the level of CD4+CD28null T lymphocyte population, and subsequently on atherosclerosis in patients with chronic renal disease. Methods We recruited 90 chronic kidney disease patients. The patients were divided into three groups according to carotid intimal medial thickness (CIMT) as an indicator of atherosclerosis. Two groups (group A in whom CIMT above 0.95 mm and B in whom CIMT below 0.95 mm) were given statin (atorvastatin 20mg) while the third group (group C in whom CIMT below 0.95 mm) continue only on the conservative treatment for CKD patients. CD4+CD28null T cells was measured in the three groups at the beginning of the study and after 6 months of statin therapy. Results CD4+CD28null T cells was decreased in statin groups (group A and B) when compared to no-statin group (group C) at the end of the study. Multivariable regression analysis for the effect of statin therapy showed that statin can independently increase the percentage of decrease both CD4+CD28null cells at the end of our study (p-value <0.0001). Conclusion Our study demonstrates that statins reduce CD4+CD28null T cells in CKD patients especially with atherosclerosis suggesting that statins may help in altering the inflammatory process that lead to atherosclerosis.
scite is a Brooklyn-based organization that helps researchers better discover and understand research articles through Smart Citations–citations that display the context of the citation and describe whether the article provides supporting or contrasting evidence. scite is used by students and researchers from around the world and is funded in part by the National Science Foundation and the National Institute on Drug Abuse of the National Institutes of Health.
hi@scite.ai
10624 S. Eastern Ave., Ste. A-614
Henderson, NV 89052, USA
Copyright © 2024 scite LLC. All rights reserved.
Made with 💙 for researchers
Part of the Research Solutions Family.