Carbonyl stress in uremia

The accumulation in uremic circulation of reactive carbonyl compounds (RCOs) generated from carbohydrates and lipids has been unraveled and recently referred to as carbonyl stress. Two mechanisms are considered to account for the cause of carbonyl stress in uremia: an increased generation or a decreased detoxification of RCOs. RCOs modify protein amino residues by nonenzymatic biochemistry and form two types of irreversible alterations of proteins: advanced glycation end products (AGEs) through the Maillard reaction and advanced lipoxidation end products (ALEs) derived from lipid peroxidation. Studies support the active contribution of carbonyl stress in uremic complications, such as atherogenesis. RCOs as well as AGEs/ALEs interfere with various cellular functions and initiate a range of cellular responses. More studies are required to elucidate the contribution of nutrition to the pathophysiology of carbonyl stress and to the eventual complications of uremia.