English (United Kingdom)

https://curated-unify.zendy.io/wp-json/zendy-region/v1/featured_content/oa?rat=en

https://curated-unify.zendy.io/wp-json/zendy-region/v1/highlighted_journal/

Global: Zendy Plus annual

Presents the access of premium content as premium feature

Premium Content

Presents the keyphrase highlighting as premium feature

Keyphrase Highlighting

Presents the summarisation as premium feature

Summarisation

Insights

Presents the pdf analysis as premium feature

PDF Analysis

Presents the zaia usage as premium feature

ZAIA

Global: Zendy Plus monthly

Global: Zendy Tools annual

Global: Zendy Tools monthly

Global: Zendy Free Plan

Oxygen-derived free radicals are highly reactive chemical species containing an unpaired electron. They are capable of reacting with lipids, proteins and nucleic acids and are thought to have a major role in the pathogenesis of a variety of diseases including atherosclerosis, diabetes and cancer. Antioxidants protect and limit free radical damage and it is the balance between free radical activity and antioxidant mechanisms that determine the potential for tissue damage [1,2]. Oxidative stress exists when there are either low levels of these antioxidants or increased production of reactive oxygen species (ROS). In chronic renal failure patients there is a high incidence of premature cardiovascular disease [3] which despite advances in renal therapy, remains one of the leading causes of death in patients with end-stage renal failure. This can be partly explained by the increased prevalence of the major cardiovascular risk factors, including diabetes, hypercholesterolaemia and hypertension. However despite this, a significant proportion of the increased cardiovascular risk remains unexplained. Oxidative stress may play a role in atherogenesis as it is thought that oxidation of polyunsaturated fatty acids in plasma lipids, particularly in low density lipoproteins (LDL), leads to modification of lysine residues on apolipoprtoein B. The resulting modified LDL particle can be taken up by the Correspondence and offprint requests to: Dr. Alexander V Crowe, The Renal Unit, 6C Link, Royal Liverpool University Hospital, Prescot Street, Liverpool L7 8XP, U.K. Tel: 0151 706 2000, Fax: 0151 706 5841, E-mail: acrowe@liverpool.ac.uk. macrophage scavenger receptor in the arterial wall [4,5], resulting in the formation of foam cells, a key early step in the initiation of the atherosclerotic plaque. This paper reviews the evidence for oxidative stress in patients with chronic renal failure, notably in those requiring maintainence haemodialysis. In addition the important therapeutic options are discussed.

The therapeutic implications of oxidative stress in patients receiving haemodialysis