Oxidative stress has a critical role in the molecular mechanisms of renal injury in several kidney diseases, and many complications of these diseases are mediated by oxidative stress, mediators, and inflammation. There is a complex relationship between these three; mostly they induce each other. While some of the diseases themselves can contribute to oxidative stress, reactive oxygen species produced by activated leukocytes and endothelial cells in sites of inflammation cause tissue damage. Inflammation is a normal reaction of organs and tissues to protect themselves against invasion(s). However, the interactions between oxidative stress, mediators, and inflammation result in glomerular damage, proteinuria, and electrolyte and volume instabilities which cause nephron loss, in the long run.

Strong evidence indicates the importance of new molecules that are able to diminish oxidative stress, mediators, and inflammation which in turn may help to decrease the prevalence of several kidney diseases. Therefore, better understanding of the molecular and clinical mechanisms of this triad could help to provide new therapeutical strategies to control several complications in renal patients.

This issue will focus on kidney diseases within this devil's triangle, specifically relating to the clinical significance of identification and prevention.

We invite investigators to contribute original research articles as well as review articles that will stimulate the continuing efforts to understand the role of this trio in kidney diseases. Potential topics include, but are not limited to:

• Induction of oxidative stress in kidney
• Importance of oxidative stress, mediators, and inflammation in endothelial dysfunction and vascular remodeling in hypertension
• New markers of oxidative stress and cellular injury in acute kidney injury
• Role of oxidative stress, mediators, and inflammation in glomerular diseases
• The relationship between uremic toxins and oxidative stress in chronic kidney disease
• Role of oxidative stress in renal aging
• New animal models to understand the roles of oxidative stress, mediators, and inflammation in kidney
• Oxidative stress pathway: what can we learn from embryology?

Before submission authors should carefully read over the journal's Author Guidelines, which are located at http://www.sage-hindawi.com/journals/ijn/guidelines/. Prospective authors should submit an electronic copy of their complete manuscript through the journal Manuscript Tracking System at http://mts.sage-hindawi.com/ according to the following timetable: