Effects of potassium citrate therapy (60 mEq/day) on urinary chemistries and crystallization were compared to those of sodium citrate treatments in five patients with uric acid lithiasis. Both alkali treatments significantly increased urinary pH (P < 0.001), from 5.35 ± 0.18 SD to 6.68 ± 0.14 for potassium citrate and 6.73 ± 0.20 for sodium citrate. During potassium citrate therapy, urinary calcium significantly declined from 154 ± 47 mg/day to 99 ± 23 mg/day (P < 0.01) and urinary citrate rose from 398 ± 119 mg/day to 856 ± 103 mg/day (P < 0.001). The urinary saturation (activity product ratio) of calcium oxalate decreased from 3.21-fold to 1.69-fold saturation (P < 0.01), and the inhibitor activity against calcium oxalate precipitation (formation product ratio) significantly increased. However, sodium citrate therapy did not significantly decrease urinary calcium (to 139 ± 24 mg/day), although it increased urinary citrate substantially (to 799 ± 89 mg/day, P < 0.01). Urinary environment became supersaturated with respect to brushite (calcium phosphate) and monosodium urate. The inhibitor activity against calcium oxalate precipitation was not significantly altered for the whole group; in two patients, it decreased by more than 30%. The results indicate that (1) both alkali therapies are equally effective in preventing uric acid stone formation because of their ability to increase urinary pH, and (2) potassium citrate may prevent the complication of calcium nephrolithiasis in patients with uric acid stones, whereas sodium citrate may not.
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