Hochreiter W, Knoll Th, Hess B
Urologische Universitätsklinik, Inselspital, Bern.
Ther Umsch. 2003 Feb;60(2):89-97. doi: 10.1024/0040-5930.60.2.89.
While calcium oxalate and calcium phosphate make up at least 80% of all kidney stones, infection-induced and uric acid stones occur in 10% and 8%, respectively. Although any type of stone may become infected, the term "infection stones" means that stone formation exclusively depends on urease-producing bacteria. The splitting of urea leads to a rise in urinary pH which may induce crystallization of struvite (magnesium-ammonium-phosphate), the major constituent of infection stones, or carbonate apatite. Struvite stones account for the majority of staghorn calculi. They can grow quite large and may fill the entire collecting system. Patients with struvite stones may present with acute flank pain or remain completely asymptomatic. The cure of infection stones requires complete removal of the stone material. For uric acid crystallization and stone formation, low urine pH (below 5.5) is a more important risk factor than increased urinary uric acid excretion. Main causes of low urine pH are tubular disorders (including gout), chronic diarrheal states or severe dehydration. Accordingly, the treatment of uric acid stones consists not only of hydration (urine volume above 2000 ml per day), but mainly of urine alkalinization to pH values between 6.2 and 6.8. Urinary uric acid excretion can be reduced by a low-purine diet as well as--in case of recurrent uric acid stones and/or gout--by allopurinol. Cystinuria is a rare hereditary gene disorders with impaired tubular reabsorption of cystine. Stone formation occurs as a consequence of cystine's relatively low solubility at urine pH levels below 8. Only symptomatic diet and drug treatments are currently available, with urine dilution and urine alkalinization being the most efficient ones. Cystine stones respond poorly to shockwave lithotripsy, so that invasive procedures may regularly be necessary. 2,8-dihydroxy-adenine stones occur as a consequence of an enzyme deficiency that involves purine metabolism. These resulting stones are not visible by fluoroscopy and are therefore often misinterpreted as uric acid stones. Low-purine diet and allopurinol reduce the frequency of stone formation.
虽然草酸钙和磷酸钙构成了所有肾结石的至少80%,但感染性结石和尿酸结石分别占10%和8%。尽管任何类型的结石都可能被感染,但“感染性结石”一词意味着结石形成完全取决于产脲酶细菌。尿素分解导致尿液pH值升高,这可能会诱导鸟粪石(磷酸镁铵)或碳酸磷灰石结晶,而鸟粪石是感染性结石的主要成分。鹿角形结石大多是鸟粪石结石。它们可以长得很大,可能会填满整个集合系统。鸟粪石结石患者可能会出现急性胁腹痛,也可能完全没有症状。感染性结石的治愈需要彻底清除结石物质。对于尿酸结晶和结石形成,低尿液pH值(低于5.5)比尿尿酸排泄增加是更重要的危险因素。低尿液pH值的主要原因是肾小管疾病(包括痛风)、慢性腹泻状态或严重脱水。因此,尿酸结石的治疗不仅包括水化(每天尿量超过2000毫升),而且主要是将尿液碱化至pH值在6.2至6.8之间。低嘌呤饮食以及(对于复发性尿酸结石和/或痛风患者)别嘌醇可以降低尿尿酸排泄。胱氨酸尿症是一种罕见的遗传性基因疾病,肾小管对胱氨酸的重吸收受损。由于胱氨酸在尿液pH值低于8时溶解度相对较低,所以会形成结石。目前只有对症饮食和药物治疗方法,尿液稀释和尿液碱化是最有效的方法。胱氨酸结石对冲击波碎石术反应不佳,因此通常可能需要采用侵入性手术。2,8 - 二羟基腺嘌呤结石是嘌呤代谢相关酶缺乏的结果。这些结石在荧光透视下不可见,因此常常被误诊为尿酸结石。低嘌呤饮食和别嘌醇可减少结石形成的频率。