Maruyama M, Yoshida E, Sugiki M, Mihara H, Sumi H, Sakai R
Department of Physiology, Miyazaki Medical College, Kihara, Japan.
Enzyme. 1991;45(1-2):54-62. doi: 10.1159/000468865.
Acid-stable trypsin inhibitor (ASTI) activity was measured during experimental acute renal tubular dysfunction and glomerulonephritis in rats. A marked elevation of ASTI activity occurred at a very early stage of acute renal tubular damage, and the changes were observed prior to histological abnormalities or elevation of blood creatinine. No alteration in ASTI activity was observed at an early stage of experimental glomerulonephritis. The data obtained confirm that ASTI is excreted through the renal tubules and that the plasma ASTI concentration is very sensitive to renal tubular dysfunction.
在大鼠实验性急性肾小管功能障碍和肾小球肾炎期间,对酸稳定的胰蛋白酶抑制剂(ASTI)活性进行了测定。在急性肾小管损伤的极早期,ASTI活性显著升高,并且在组织学异常或血肌酐升高之前就观察到了这些变化。在实验性肾小球肾炎的早期未观察到ASTI活性的改变。所获得的数据证实,ASTI通过肾小管排泄,并且血浆ASTI浓度对肾小管功能障碍非常敏感。