Baggio B, Gambaro G, Ossi E, Favaro S, Borsatti A
J Urol. 1983 Jun;129(6):1161-2. doi: 10.1016/s0022-5347(17)52619-1.
Urinary excretion of gamma-glutamyl transpeptidase, angiotensin I converting enzyme, beta-galactosidase and N-acetyl-beta-glucosaminidase was evaluated in 30 patients with idiopathic calcium oxalate urolithiasis. Higher than normal values were observed and the excretory enzyme pattern suggested tubular damage in patients with stones. A parallel study in the rat showed that an oxalate surcharge can promote increased urinary excretion of these enzymes. It is known that urothelium injury may enhance crystal adhesion. If the damage is primary it may be viewed as a promoting factor. If it is secondary it may be considered a factor capable of increasing salt precipitation.
对30例特发性草酸钙尿路结石患者的γ-谷氨酰转肽酶、血管紧张素I转换酶、β-半乳糖苷酶和N-乙酰-β-氨基葡萄糖苷酶的尿排泄情况进行了评估。观察到这些值高于正常水平,且排泄酶模式提示结石患者存在肾小管损伤。在大鼠身上进行的一项平行研究表明,草酸盐超载可促进这些酶的尿排泄增加。已知尿路上皮损伤可能会增强晶体黏附。如果损伤是原发性的,它可能被视为一个促进因素。如果是继发性的,它可能被认为是一个能够增加盐沉淀的因素。