Pedraza-Chaverrí J, Cruz C, Larriva-Sahd J, Juárez R M, Orozco H, Hernández-Pando R, Tapia E
Departamento de Biologia, Facultad de Química, UNAM, México, DF, México.
Ren Fail. 1995 Jul;17(4):365-75. doi: 10.3109/08860229509037602.
Angiotensin I converting enzyme (ACE) activity was measured in serum, urine, and tissues of rats with acute renal failure (ARF) induced by glycerol. Glycerol-injected rats were subdivided in three groups according to the urinary volume: oliguric, nonoliguric, and polyuric. The damage to the proximal tubule was evident by (a) the histological analysis at light and electron microscopy level, (b) the augmented urinary excretion of the enzymes dipeptidyl aminopeptidase IV and N-acetyl-beta-D-glucosaminidase, and (c) the low molecular weight proteinuria pattern. On the other hand, the appearance of the glomeruli at the ultrastructural level was normal. These data suggest that the increased urinary excretion of enzymes and proteins in these rats is a consequence of the tubular injury. ARF was markedly higher in the oliguric rats. Urine ACE activity increased in the rats of the three groups, but statistical significance was reached only in the oliguric rats. Serum ACE activity increased in the oliguric rats and tissue ACE activity did not change. It is concluded that the high urinary ACE in glycerol-treated rats is associated with the damage to the kidney tubules. These data support the contention that urinary ACE may be another marker of injury to the proximal tubule.
在甘油诱导的急性肾衰竭(ARF)大鼠的血清、尿液和组织中测量了血管紧张素I转换酶(ACE)活性。根据尿量将注射甘油的大鼠分为三组:少尿组、非少尿组和多尿组。通过以下方面可明显看出近端小管受损:(a)光镜和电镜水平的组织学分析;(b)二肽基氨基肽酶IV和N-乙酰-β-D-氨基葡萄糖苷酶的尿排泄增加;(c)低分子量蛋白尿模式。另一方面,肾小球在超微结构水平的外观正常。这些数据表明,这些大鼠中酶和蛋白质尿排泄增加是肾小管损伤的结果。少尿大鼠的急性肾衰竭明显更严重。三组大鼠的尿ACE活性均升高,但仅少尿组达到统计学显著性。少尿大鼠的血清ACE活性升高,而组织ACE活性未改变。结论是,甘油处理大鼠的高尿ACE与肾小管损伤有关。这些数据支持尿ACE可能是近端小管损伤的另一个标志物的观点。