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Updated: Aug 30, 2026

A Mouse 5/6th Nephrectomy Model That Induces Experimental Uremic Cardiomyopathy
Published on: November 7, 2017
[Oxidative stress in chronic renal failure and hemodialysis]
B Descamps-Latscha1, V Witko-Sarsat
1INSERM U507, Hôpital Necker, Paris. b.descamps@necker.fr
Abstract:
Evidence has accumulated that oxidative stress resulting from the increased generation of oxidants (reactive oxygen species and chlorinated oxidants) by activated phagocytes at the contact of dialysis membranes and dialysate endotoxins and from the uremia-related profound deficiency in antioxidants (glutathion system mainly) plays a prominent role in the pathogenesis of the accelerated atherosclerosis process which accounts for almost one half of deaths in dialysis patients. However more recent studies of large cohorts of uremic patients have shown that oxidative stress is already present at an early stage of chronic renal failure, increases with the progression of uremia and that phagocytic cells are elective targets of uremic toxins. Our recent studies aimed at better characterizing oxidative stress in dialysis patients have led to describe the presence in the plasma of uremic patients of AOPP (Advanced Oxidation Protein Products) which proved to be potential uremic toxins and mediators of inflammation. A better knowledge of the respective contribution of bioincompatibility and uremic toxins at the origin of phagocyte activation will allow to develop therapeutic strategies aimed at reducing the incidence of oxidative stress related complications and with AOPP as a gauge of their efficacy.
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