Abstract
Renal failure is accompanied by progressive muscle weakness and premature fatigue, in part linked to hypokinesis and in part to uremic toxicity. These changes are associated with various detrimental biochemical and morphological alterations. All of these pathological parameters are collectively termed uremic myopathy. Various interventions while helpful can't fully remedy the pathological phenotype. Complex mechanisms that stimulate muscle dysfunction in uremia have been proposed, and oxidative stress could be implicated. Skeletal muscles continuously produce reactive oxygen species (ROS) and reactive nitrogen species (RNS) at rest and more so during contraction. The aim of this mini review is to provide an update on recent advances in our understanding of how ROS and RNS generation might contribute to muscle dysfunction in uremia. Thus, a systematic review was conducted searching PubMed and Scopus by using the Cochrane and PRISMA guidelines. While few studies met our criteria their findings are discussed making reference to other available literature data. Oxidative stress can direct muscle cells into a catabolic state and chronic exposure to it leads to wasting. Moreover, redox disturbances can significantly affect force production per se. We conclude that oxidative stress can be in part responsible for some aspects of uremic myopathy. Further research is needed to discern clear mechanisms and to help efforts to counteract muscle weakness and exercise intolerance in uremic patients.
Highlights
Among the clinical entities affecting thousands of patients, chronic kidney disease (CKD) is a silent epidemic expected to influence more than 50% of the Americans born today (Grams et al, 2013) and approximately 40% of the population in Europe (Zoccali et al, 2010)
Lim et al (2002a) found increased malondialdehyde (MDA) and protein carbonyls (PC) levels reflecting extensive oxidative damage to total protein content and lipids, in muscle suggested by the authors to be due to increased levels of inflammatory cytokines and to increased protein degradation
Increased levels of lipid peroxidation in blood samples of CKD patients during HD treatment has been found elsewhere (Varan et al, 2010) and could enhance the susceptibility of LDL oxidation which is a major contributor in the genesis of atherosclerosis
Summary
Among the clinical entities affecting thousands of patients, chronic kidney disease (CKD) is a silent epidemic expected to influence more than 50% of the Americans born today (Grams et al, 2013) and approximately 40% of the population in Europe (Zoccali et al, 2010). Biochemical and nutritional changes occurring through the progression of CKD can stimulate protein losses and can contribute to the development of muscle wasting This has grave significance as catabolic conditions increase the risk of morbidity and mortality (Griffiths, 1996; Gordon et al, 2007). Oxidative stress promotes catabolic state and accelerates muscle atrophy (Moylan and Reid, 2007) It can affect contractility of the available muscle and sarcomeric protein expression. The decrease in Ca2+ sensitivity which contributes to muscle fatigue is considered as an acute effect of oxidative stress (Lamb and Westerblad, 2011). Based on recent advances in our understanding of how ROS and RNS affect muscle function, this mini-review aimed to examine if oxidative stress can contribute to muscle dysfunction in ESRD
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