Coe F L, Strauss A L, Tembe V, Le Dun S
Kidney Int. 1980 May;17(5):662-8. doi: 10.1038/ki.1980.205.
Hyperuricosuria appears to cause calcium oxalate nephrolithiasis by promoting the formation of monosodium urate or uric acid crystals, which either act as seed crystals for calcium oxalate or adsorb normally occurring macromolecular inhibitors of calcium oxalate crystallization. Both mechanisms require that hyperuricosuria cause excessive supersaturation of the urine, but this has not yet been studied under conditions of normal lifestyle. We have measured the saturation with respect to sodium hydrogen urate and the concentration of undissociated uric acid in the urine samples of 67 patients with calcium nephrolithiasis, who had idiopathic hypercalciuria, hyperuricosuria, both, or neither disorder. Patients with hyperuricosuria excreted urine that was supersaturated with respect to monosodium urate or undissociated uric acid more frequently than did other stone formers or normal subjects, and are therefore at a greater risk of forming a solid phase of monosodium urate or uric acid. Treatment measures that lowered uric acid excretion also lowered urine saturation, and this may be the reason that such treatment tends to prevent calcium stone recurrence.
高尿酸尿症似乎通过促进尿酸钠或尿酸晶体的形成而导致草酸钙肾结石，这些晶体要么作为草酸钙的晶种，要么吸附正常存在的草酸钙结晶大分子抑制剂。这两种机制都要求高尿酸尿症导致尿液过度饱和，但在正常生活方式的条件下尚未对此进行研究。我们测量了67例患有草酸钙肾结石的患者尿液样本中尿酸氢钠的饱和度和未离解尿酸的浓度，这些患者患有特发性高钙尿症、高尿酸尿症、两者皆有或两者皆无。与其他结石形成者或正常受试者相比，高尿酸尿症患者排出的尿液中尿酸钠或未离解尿酸处于过饱和状态的频率更高，因此形成尿酸钠或尿酸固相的风险更大。降低尿酸排泄的治疗措施也降低了尿液饱和度，这可能是此类治疗倾向于预防钙结石复发的原因。
