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[肾小球肾炎患者尿液中的胰蛋白酶抑制剂]

[Trypsin inhibitor in the urine of patients with glomerulonephritis].

作者信息

Paskhina T S, Platonova L V, Poliantseva L R

出版信息

Vopr Med Khim. 1988 Jan-Feb;34(1):89-94.

PMID:3369132
Abstract

Concentrations of urinary trypsin inhibitor (UTI) and acid stable antitryptic activity (AS-ATA) were estimated in morning urine of 50 patients with chronic glomerulonephritis and of 13 healthy persons in order to detect interrelationship between severity of kidney impairment and the content of the inhibitor in urine. In healthy persons concentrations of UTI and AS-ATA were equal to 1.05 +/- 0.15 micrograms/ml and 0.12 +/- 0.04 IU/ml, respectively. Similar values of the substances were detected in patients with latent form of glomerulonephritis and normal kidney function. Statistically distinct (P less than 0.01) increase of both these inhibitors was found in urine of patients with latent form of glomerulonephritis and impaired kidney function (4.77 +/- 1.24 micrograms/ml and 0.39 +/- 0.15 IU/ml, respectively) as well as with nephrotic form (26.17 +/- 7.55 micrograms/ml and 1.37 +/- 0.35 IU/ml, respectively) of glomerulonephritis of both primary type and caused by accompanying systemic diseases. Further increase in concentration of UTI up to 31.74 +/- 7.38 micrograms/ml and activation of AS-ATA in urine was observed in the patients with nephrotic form of glomerulonephritis at the step of chronic kidney insufficiency. The increase in UTI concentration observed did not correlate with the level of leukocyturia. Proteinases of monocytes, mast cells, fibroblasts, involved in inflammation and formation of connective tissue in kidney, but not of enzymes from polymorphonuclear leukocytes, appear to be responsible for formation of UTI out of its precursor inter-alpha-trypsin inhibitor in glomerulonephritis.

摘要

为检测肾功能损害严重程度与尿中抑制剂含量之间的相互关系,对50例慢性肾小球肾炎患者及13名健康人的晨尿进行了尿胰蛋白酶抑制剂(UTI)和酸稳定抗胰蛋白酶活性(AS - ATA)浓度的测定。健康人尿中UTI和AS - ATA浓度分别为1.05±0.15微克/毫升和0.12±0.04国际单位/毫升。在隐匿型肾小球肾炎且肾功能正常的患者中也检测到了这些物质的相似值。在隐匿型肾小球肾炎且肾功能受损的患者(分别为4.77±1.24微克/毫升和0.39±0.15国际单位/毫升)以及原发性和由伴随全身性疾病引起的肾病型肾小球肾炎患者(分别为26.17±7.55微克/毫升和1.37±0.35国际单位/毫升)的尿中,发现这两种抑制剂均有统计学显著升高(P<0.01)。在肾病型肾小球肾炎患者处于慢性肾功能不全阶段时,观察到尿中UTI浓度进一步升高至31.74±7.38微克/毫升,且AS - ATA被激活。观察到的UTI浓度升高与白细胞尿水平无关。在肾小球肾炎中,参与肾脏炎症和结缔组织形成的单核细胞、肥大细胞、成纤维细胞的蛋白酶,而非多形核白细胞的酶,似乎是由其前体α - 胰蛋白酶抑制剂形成UTI的原因。

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