Abstract
The excessive activation of the renin-angiotensin system in kidney disease leads to alteration of intracellular pathways which concur altogether to the induction of cardiovascular and renal remodeling, exposing these patients since the very beginning of the renal injury to chronic kidney disease and progression to end stage renal disease, a very harmful and life threatening clinical condition. Oxidative stress plays a pivotal role in the pathophysiology of renal injury and cardiovascular-renal remodeling, the long-term consequence of its effect. This review will examine the role of oxidative stress in the most significant pathways involved in cardiovascular and renal remodeling with a focus on the detrimental effects of oxidative stress-mediated renal abnormalities on the progression of the disease and of its complications. Food for thoughts on possible therapeutic target are proposed on the basis of experimental evidences.
Highlights
Oxidative stress arises when the physiologically-produced oxidant species overwhelm the endogenous antioxidant recovery capacity of the cells, leading to loss of intracellular redox homeostasis [1]
In a cohort of post- renal transplant hypertensive patients from our Unit, we observed a significant increase of p22phox expression in addition to reduced antioxidant defenses such as heme oxygenase isoform-1 (HO-1) and total plasma antioxidant power when compared to normotensive transplanted recipients [51]
Good evidence of this may come from a study in our cohort of patients with kidney failure undergoing dialysis with a vitamin E-coated dialyzer, where we observed that one year of treatment decreased significantly the expression of oxidative stress and inflammation proteins and related markers associated with cardiovascular disease [47]
Summary
Oxidative stress arises when the physiologically-produced oxidant species overwhelm the endogenous antioxidant recovery capacity of the cells, leading to loss of intracellular redox homeostasis [1]. In kidney disease, the excessive activation of the RAS and the excessive presence of oxidative stress participate together as playing a game in the progression of structural changes in the vessels and in the heart. Both oxidative stress and RAS are very active players in a fight between endogenous antioxidant defenses, oxidative stress and its mediators where progressive renal functional decline remains the natural most frequent result if no approach both pharmacologic and nutritional is started (Figure 1).
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