Pak C Y, Peterson R
Arch Intern Med. 1986 May;146(5):863-7.
Calcium stone (renal) formation in patients with hyperuricosuria has been ascribed to the urate-induced crystallization of calcium oxalate. Citrate (0.5mM), added to synthetic medium metastably supersaturated with respect to calcium oxalate, was shown to inhibit heterogeneous nucleation of calcium oxalate by monosodium urate (2 mg/mL). Long-term trial with potassium citrate (60 to 80 mEq/day) was therefore undertaken to determine whether induced hypercitraturia would prevent calcium oxalate stone formation in 19 patients with hyperuricosuria. The treatment produced a sustained rise in urinary pH by 0.55 to 0.85 to the high normal range (6.5 to 7.0). Urinary citrate levels rose by 249 to 402 mg/day to approximate the normal mean value of 643 mg/day. Commensurate with these changes, urinary saturation of calcium oxalate (relative saturation ratio) and the amount of undissociated uric acid declined significantly. However, the urinary uric acid and saturation of monosodium urate remained elevated. Stone formation declined from 1.55 +/- 2.70 per patient-year to 0.38 +/- 1.22 per patient-year during mean treatment period of 2.35 +/- 0.88 years. Stones ceased to form in 16 of 19 patients during treatment. The results provide physicochemical and clinical evidence for the utility of potassium citrate in the management of hyperuricosuric calcium oxalate nephrolithiasis.
高尿酸尿症患者的钙结石（肾结石）形成被归因于尿酸盐诱导的草酸钙结晶。向相对于草酸钙呈亚稳过饱和的合成培养基中添加柠檬酸盐（0.5mM），结果显示其可抑制尿酸钠（2mg/mL）诱导的草酸钙异质成核。因此，对19例高尿酸尿症患者进行了柠檬酸钾（60至80mEq/天）的长期试验，以确定诱导高柠檬酸尿症是否能预防草酸钙结石形成。该治疗使尿液pH值持续升高0.55至0.85，达到高正常范围（6.5至7.0）。尿柠檬酸盐水平升高249至402mg/天，接近正常平均值643mg/天。与这些变化相应，草酸钙的尿饱和度（相对饱和比）和未离解尿酸的量显著下降。然而，尿酸和尿酸钠的尿饱和度仍保持升高。在平均2.35±0.88年的治疗期内，结石形成从每位患者每年1.55±2.70次降至0.38±1.22次。19例患者中有16例在治疗期间停止形成结石。这些结果为柠檬酸钾在治疗高尿酸尿性草酸钙肾结石中的效用提供了物理化学和临床证据。
