[{"from": "human", "value": "Provide a description of this molecule. [C][=C][N][Branch2][Ring1][#Branch2][C][=N][C][=Branch1][Branch2][=N][C][Ring1][Branch1][=C][Ring1][=Branch2][N][C][C][C][C@@H1][Branch1][=Branch1][C][=Branch1][C][=O][O][N][C][C][C][C][C@@H1][Branch1][=Branch1][C][=Branch1][C][=O][O][N]"}, {"from": "gpt", "value": "The molecule is a uremic toxin.  Uremic toxins can be subdivided into three major groups based upon their chemical and physical characteristics: 1) small, water-soluble, non-protein-bound compounds, such as urea; 2) small, lipid-soluble and/or protein-bound compounds, such as the phenols and 3) larger so-called middle-molecules, such as beta2-microglobulin. Chronic exposure of uremic toxins can lead to a number of conditions including renal damage, chronic kidney disease and cardiovascular disease. \nPentosidine is a carbohydrate-derived advanced glycation end products (AGEs) that is considerably elevated in uremic patients. Derived from ribose, a pentose, pentosidine forms fluorescent cross-links between the arginine and lysine residues in collagen. It is formed in a reaction of the amino acids with the Maillard reaction products of ribose. Although it is present only in trace concentrations among tissue proteins, it is useful for assessing cumulative damage to proteins-advanced glycation endproductsThis compound per se has no biological activities but is highly correlated to the levels of precursors of carbonyl compounds, and for this reason is considered a reliable surrogate marker for AGEs. The modification of proteins in uremia is not limited to AGEs, since advanced lipoxidation end products are also demonstrable in plasma proteins in uremia. The accumulation of these compounds does not seem to be dependent only on the decline of renal function. Carbonyl precursors of AGEs and advanced lipoxidation end products are markedly elevated in uremic patients. Preliminary cross-sectional studies in haemodialysis patients seem to indicate that the AGEs and carbonyl stress may be involved in the pathogenesis of alterations in left ventricular geometry and function in these patients. The plasma pentosidine level in diabetic nephropathy was found to be determined by factors such as renal function control of glucose and the patient's age; of these, renal function was the most critical factor. The pathological role of AGEs in diabetic nephropathy, is in the expanded mesangial area of diffuse diabetic glomerulosclerosis, with nodular lesions, characteristic of diabetic nephropathy. These suggests a potential link of AGEs accumulation, which may be determined by renal function, control of glucose and age, to renal tissue damage in diabetic nephropathy. The rate of accumulation of glycoxidation products is accelerated in diabetes and age-adjusted concentrations of two advanced glycation end-products (AGE) in tissue proteins, N(6)-carboxymethyllysine and pentosidine, correlate with the severity of complication in diabetic patients. (A3291, A3292, A3293)."}]