Clinical signs and symptoms of end-stage renal failure patients are at least in part related to the accumulation of uremic retention solutes and uremic toxins. This article describes abnormalities caused by asymmetric dimethylarginine, advanced glycation end products, advanced lipoxidation end products, advanced oxidation protein products, homocysteine as well as low and high molecular weight inhibitors of polymorphonuclear leukocytes. Mechanisms for the accumulation of uremic retention solutes and uremic toxins include decrease of renal function, oxidative stress, microinflammation and/or uremia per se resulting in protein modifications with new biological functions.