Although the etiologic role of microcrystalline monosodium urate monohydrate in the pathogenesis of acute gouty arthritis has been well established, the mechanism by which urate precipitates in joints, soft tissues and the kidneys remains unclear. Some studies have suggested that the solubility of urate is the key factor and that when the solubility of urate in blood synovial fluid and urine is exceeded, urate then precipitates. The question is more complex than this, however, since only approximately 25 per cent of patients with hyperuricemia develop acute gouty arthritis. Furthermore, there is poor correlation between uric acid concentration and the frequency of acute gouty attacks. This has led to speculation that there are factors in serum which are partially responsible for solubilization of urate and that alterations in these factors could be responsible for urate deposition.

Related Organizations

University of California, Los Angeles
United States

Keywords

Binding Sites, Aspirin, Gout, Probenecid, Allopurinol, Indomethacin, Osmolar Concentration, Blood Proteins, Hydrogen-Ion Concentration, Kinetics, Phenylbutazone, Solubility, Evaluation Studies as Topic, Methods, Humans, Kidney Diseases, Colchicine, Dialysis, Serum Albumin, Protein Binding

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