Reactive carbonyl compounds related uremic toxicity ("carbonyl stress").

Many studies on uremic toxins have focused on enzymatic biochemistry. Recently, attention has turned to nonenzymatic biochemistry, especially progressive and irreversible modifications of proteins. Two different approaches opened the field of irreversible nonenzymatic modifications of proteins in uremia: the advanced glycation end products (AGEs) derived from the Maillard reaction and the advanced lipoxidation end products (ALEs) derived from lipid peroxidation. They have revealed the accumulation of reactive carbonyl compounds (RCOs) derived from carbohydrates and lipids and the subsequent carbonyl modifications of proteins ("carbonyl stress"). In this article, we describe the causal role of various RCOs and AGEs/ALEs accumulating in uremia, the clinical consequences of carbonyl stress in uremia, and finally, the therapeutic perspectives. We propose carbonyl stress as a new uremic toxicity.