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目的观察激肽系统与糖尿病肾病的关系。方法用比色法测定激肽释放酶（ＴＫＡ）活性，用ＨＯＥ１４０和胰激肽释放酶改变激肽系统的功能。结果１８周时糖尿病组ＴＫＡ活性明显低于８周时的水平（Ｐ＜０．０１），与正常对照组比较有极显著差异（Ｐ＜０．０００１）。胰激肽释放酶治疗组ＴＫＡ活性升高（Ｐ＜０．０５），该组病变较糖尿病组轻。结论糖尿病可抑制激肽系统的活性，而补充胰激肽释放酶对糖尿病肾病的发展有一定的抑制作用。
Objective To observe the relationship between kinin system and diabetic nephropathy. Methods The activity of kallikrein (TKA) was assayed by colorimetric assay and the function of kinin system was altered by HOE140 and kallikrein. Results TKA activity in diabetic group was significantly lower than that at 8 weeks (P <0.01) at 18 weeks, which was significantly different from that in normal control group (P <0.0001). The activity of TKA in pancreatic kallikrein group was higher than that in diabetic group (P <0.05). Conclusion Diabetes can inhibit the activity of kinin system, while the addition of kallikrein has some inhibitory effect on the development of diabetic nephropathy.