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Review
. 2015:2015:806358.
doi: 10.1155/2015/806358. Epub 2015 Mar 15.

Chronic kidney disease influences multiple systems: describing the relationship between oxidative stress, inflammation, kidney damage, and concomitant disease

Patrick S Tucker  1 , Aaron T Scanlan  1 , Vincent J Dalbo  1
Affiliations
Review

Chronic kidney disease influences multiple systems: describing the relationship between oxidative stress, inflammation, kidney damage, and concomitant disease

Patrick S Tucker et al. Oxid Med Cell Longev. 2015.

Abstract

Chronic kidney disease (CKD) is characterized by increased levels of oxidative stress and inflammation. Oxidative stress and inflammation promote renal injury via damage to molecular components of the kidney. Unfortunately, relationships between inflammation and oxidative stress are cyclical in that the inflammatory processes that exist to repair radical-mediated damage may be a source of additional free radicals, resulting in further damage to renal tissue. Oxidative stress and inflammation also have the ability to become systemic, serving to injure tissues distal to the site of original insult. This review describes select mediators in the exacerbatory relationship between oxidative stress, inflammation, and CKD. This review also discusses oxidative stress, inflammation, and CKD as they pertain to the development and progression of common CKD-associated comorbidities. Lastly, the utility of several widely accessible and cost-effective lifestyle interventions and their ability to reduce oxidative stress and inflammation are discussed and recommendations for future research are provided.

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Figures

Figure 1
Figure 1
Radical reactions leading to initial renal injury. Intermediates in grey are harmful to biological molecules. Compounds in white, although not directly damaging, are involved in harmful reactions.
Figure 2
Figure 2
Interactions between radical damage, inflammation, and renal injury. Intermediates in grey initiate damage of the molecular components of renal tissue. Compounds in white, although not directly damaging, are involved in harmful reactions. Damage resulting from intermediates in grey promotes an inflammatory response during which additional superoxide is released via phagocytic NADPH oxidase activity.
Figure 3
Figure 3
Interactions between radical damage, inflammation, and distal injury. Intermediates in grey initiate damage of the molecular components of renal tissue. Compounds in white, although not directly damaging, are involved in harmful reactions. Damage resulting from intermediates in grey promotes an inflammatory response during which additional superoxide is released via phagocytic NADPH oxidase activity. If sustained, this process may lead to a systemic inflammatory response that can result in damage to tissues that are distal to the kidney, such as the pancreas (type 2 diabetes) and vasculature (cardiovascular disease), via related increases in the production of reactive oxygen species (ROS). For example, the transcription of NF-κB-dependent genes may regulate levels of cellular ROS; the NF-κB pathway may be activated by stimulation of proinflammatory receptors, such as the TNF receptor superfamily. In turn, NF-κB activation may also be regulated by cellular levels of ROS; ROS can activate NF-κB through alternative IκB phosphorylation, resulting in the degradation of IκB.
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