Eighteen patients with uric acid nephrolithiasis (six with uric acid stones alone and 12 with both uric acid and calcium stones) underwent long-term treatment (1 to 5.33 years, mean of 2.78 years) with potassium citrate (30 to 80 mEq/day, usually 60 mEq/day). Urinary pH increased from low (5.30 ± 0.31 SD) to normal (6.19 to 6.46) during treatment. Urinary content of undissociated uric acid, which was high to begin with at 204 ± 82 mg/day, decreased to the normal range (64 to 108 mg/day) following treatment. Urinary citrate rose from 503 ± 225 mg/day to 852 to 998 mg/day. Urinary saturation of calcium oxalate significantly declined with potassium citrate treatment. New stone formation rate declined from 1.20 ± 1.68 stones/year to 0.01 ± 0.04 stones/year (P < 0.001 by chi square). Remission was experienced in 94.4% of patients, and the group stone formation rate declined by 99.2%. Detailed case reports were obtained in five patients showing different responses between sodium alkali and potassium alkali treatment. All five patients had persistently low urinary pH (typically < 5.5) and normouricosuria, and four had hyperuricemia. Before treatment, they had stones surgically removed or spontaneously passed, which were pure uric acid in composition. When sodium alkali was give (as bicarbonate or citrate, 60 to 118 mEq/day), new stone formation continued in four patients, and a radiolucent (uric acid) calculus become 'calcified' in the remaining patient. The stone analysis disclosed calcium oxalate in five patients and calcium phosphate in three patients. When potassium citrate (in four cases) or potassium bicarbonate (in one case) was offered instead over 1 to 3.5 years (at a dosage of 60 to 80 mEq/day), no new stones were formed. The results provide physiological and physicochemical rationale, as well as therapeutic efficacy for potassium citrate treatment in the management of uric acid lithiasis presenting with/without calcium stones.
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