Griffith D P, Musher D M, Itin C
Invest Urol. 1976 Mar;13(5):346-50.
Previous reports have suggested that urease-producing bacteria play a prominent role in the formation of infection-induced urinary stones. We have carried out crystalization experiments in vitro which show that bacterial urease alkalinizes urine, thereby causing: (i) supersaturation with respect to struvite and calcium phosphate; and (ii) formation of struvite and apatite crystals. Growth of Proteus in urea-free urine or in urine which contained a urease inhibitor did not cause alkalinization, supersaturation, or crystallization of struvite and apatite. Growth of Klebsiella, Escherichia coli, or Pseudomonas was not associated with significant alkalinization, supersaturation, or crystallization. Struvite and apatite crystals dissolved in Proteus-infected urine in which undersaturation was maintained by urease inhibition. Similar results in all experiments were obtained using human urine and a synthetic urine which was devoid of matrix, pyrophosphate, or other undefined solutes. Urease-induced supersaturation appears to be the primary cause of infection-induced urinary stones.
先前的报告表明,产脲酶细菌在感染性尿路结石的形成中起重要作用。我们进行了体外结晶实验,结果表明细菌脲酶使尿液碱化,从而导致:(i)相对于鸟粪石和磷酸钙过饱和;(ii)鸟粪石和磷灰石晶体形成。变形杆菌在无尿素尿液或含有脲酶抑制剂的尿液中生长不会导致尿液碱化、过饱和或鸟粪石和磷灰石结晶。克雷伯菌、大肠杆菌或假单胞菌的生长与显著的碱化、过饱和或结晶无关。鸟粪石和磷灰石晶体溶解于变形杆菌感染的尿液中,通过抑制脲酶维持不饱和状态。使用人类尿液和不含基质、焦磷酸盐或其他未定义溶质的合成尿液在所有实验中均获得了类似结果。脲酶诱导的过饱和似乎是感染性尿路结石的主要原因。