Abstract
AbstractOxidative stress is central to many pathological kidney processes. Redox states in the kidney determine the levels of oxidative stress as well as functional status of the various cell types in the kidney. Excessive generation of free radicals under the influence of certain cellular, extracellular, and environmental cues tilts the balance of redox toward damaging processes. For example, the renin-angiotensin-aldosterone system can be turned on excessively, leading to generation of free radicals in the form of superoxide anion, which is one of the potent oxidizing agents. Oxidation of lipids, proteins and even nitric oxide can lead to further generation of cell damaging products. Dyslipidemia has been shown to be intricately involved in the generation of oxidative stress. Statins improve dyslipidemia through the blockade of 3-hydroxy-3-methylglutaryl coenzyme A reductase and through decreased participation of downstream moieties in the generation of oxidative stress. In addition, statins affect the activation of transcription factors such as nuclear factor κB to mediate their anti-inflammatory and antifibrotic effects. This “pleiotropism” is important in contributing to statins overall salutary effects in chronic kidney disease.KeywordsDyslipidemiaChronic kidney diseaseOxidative stress
Sign-in/Register to access full text options 
Free) 
Talk to us
Join us for a 30 min session where you can share your feedback and ask us any queries you have
Schedule a call
