JAMES R. KLINENBERG, M.D., F.A.C.P.; RODNEY BLUESTONE, M.B., M.R.C.P.; LEE SCHLOSSTEIN, M.D.; JERRY WAISMAN, M.D.; MICHAEL W. WHITEHOUSE, D. Phil.
Hyperuricemia may be associated with various diseases; clinical gout occurs when urate crystals deposit from supersaturated body fluids. Although all the factors responsible for urate deposition are not yet known, local pH, ionic strength, and temperature, as well as the influence of protein-binding of urate, have received attention recently. The binding of urate to plasma protein may influence not only urate deposition but also the renal excretion of uric acid. Many drugs interfere with this plasma-urate binding; all these agents are uricosuric. An experimental model of gouty nephropathy in the rat has been developed to explore further the relations between hyperuricemia, plasmaurate binding, and deposition of urate in the kidney.
KLINENBERG JR, BLUESTONE R, SCHLOSSTEIN L, et al. Urate Deposition Disease: How Is It Regulated and How Can It Be Modified?. Ann Intern Med. 1973;78:99–111. doi: https://doi.org/10.7326/0003-4819-78-1-99
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Published: Ann Intern Med. 1973;78(1):99-111.
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