Azotemia and urolithiasis as outcomes of gout or hyperuricemia were examined in several ways. Azotemia occurred in two (1.8 per cent) of 113 patients with asymptomatic hyperuricemia followed for eight years and in four (2.1 per cent) of 193 normouricemic control subjects; it was mild in all instances. Azotemia was also mild when it occurred in 168 patients with gout followed for 10 years and was unrelated to the degree of control of serum uric acid levels in these patients. Projected degrees of azotemia after 40 years of sustained hyperuricemia were mild and probably of no clinical significance until levels of serum uric acid reached 10 mg/100 ml in women and 13 mg/100 ml in men. Among 1,356 men, aged 60 to 69 years when serum uric acid was measured, follow-up for 10 years showed no death from renal failure that was attributable to hyperuricemia. Risks of urolithiasis were small; approximately one stone per 295 patients per year in those with asymptomatic hyperuricemia compared with one stone per 852 patients per year in normouricemic control subjects, and one stone per 114 patients per year in those with established gout. Among the gouty patients, initial level of serum uric acid was not a predictor of stone; significantly more of those in whom urolithiasis developed were taking medication to lower serum uric acid levels than in those not taking such medicine, but the differences between those taking probenecid and those taking allopurinol were not significant. Also, among the gouty patients, the control of serum uric acid levels was similar in those in whom stones developed and in those in whom they did not. It is concluded that (1) azotemia attributable to hyperuricemia is generally mild and probably of no clinical importance until serum uric acid levels reach 13 mg/100 ml in men and 10 mg/100 ml in women; and (2) the risk of urolithiasis is sufficiently low to justify awaiting the occurrence of the first stone before commencing drug therapy to lower serum uric acid levels.
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