It has long been appreciated that the typical case of gout is preceded by an asymptomatic interval, during which the serum urate concentration is elevated.1 At a normal body fluid pH of 7.4, almost 99% of the "uric acid" exists as monovalent urate. A strikingly low solubility accounts for the propensity of its sodium salt, monosodium urate (MSU), to precipitate and elicit articular attacks, as well as form tophi.
Before effective treatment was available, the natural history of gout was chronicled extensively.1 The clinical picture included a propensity toward the development of premature hypertension and vascular disease, accompanied by an increased incidence of strokes and other sequelae. In addition, advanced renal insufficiency figured prominently in morbidity and mortality in about 20% of cases.2 Renal pathologic changes included interstitial fibrosis and MSU crystal deposition, and vascular disease with glomerular and tubular obsolescence. However, the renal prognosis in gout