Paskhina T S, Poliantseva L R, Krinskaia A V, Belolipetskaia Iu G, Nartikova V F
Vopr Med Khim. 1977 Mar-Apr;23(2):241-51.
Main components of kinin system, the arginine-esterase activity and proteinase inhibitors were estimated in blood serum of patients with nephrotic syndrome of various etiology (glomerulonephritis, amyloidosis, systemic lupus erythematous) and also in patients with latent nephritis and in healthy donors. Content of all the kinin system components (kallikreinogen, kininogen and kininase 1) proved to be increased in all the forms of nephropathy studied. Free kallikrein was found in blood serum of patients with nephrotic syndrome as distinct from healthy persons and patients with latent nephritis. The arginine-esterase activity, which shows the level of trypsin-like proteinases, was altered dissimilarly, depending on the nephrotic syndrome etiology: it was maximally increased in nephrotic syndrome of amyloid genesis and decreased in patient with systemic lupus erythematosus. High content of kallikrein and kininase I with simultaneous decrease in kininogen was typical for patients with severe form of nephrotic syndrome. Impairment of kidney in nephrotic syndrome was also characterized by an increase in alpha1-antitrypsin and in the total antitryptic activity, which reached the maximal value in nephrotic syndrome of the I degree and decreased at the II degree of the disease. In nephrotic syndrome content of alpha2-macroglobulin was maximally increased at the II degree of nephrotic syndrome and decreased in severe form of the disease. The primary alteration in content of proteinase inhibitors and high level of kinin system components were assumed to determine the conditions for activation of kinin system in blood serum and to impair the nephrotic syndrome pathogenesis, which was complicated by systemic manifestations. High content of kinin system components was apparently determined by the increased synthesis in liver tissue in response to inflammation and massive proteinuria; kininase I and alpha2-macrolgobulin, as proteins with high molecular weight, were likely to be selectively retained in blood circulation when the capillary penetration was increased.
对各种病因(肾小球肾炎、淀粉样变性、系统性红斑狼疮)的肾病综合征患者、隐匿性肾炎患者及健康供体的血清中激肽系统的主要成分、精氨酸酯酶活性和蛋白酶抑制剂进行了评估。结果表明,在所研究的所有肾病形式中,激肽系统所有成分(激肽释放酶原、激肽原和激肽酶1)的含量均升高。与健康人和隐匿性肾炎患者不同,在肾病综合征患者的血清中发现了游离激肽释放酶。显示胰蛋白酶样蛋白酶水平的精氨酸酯酶活性变化各异,取决于肾病综合征的病因:在淀粉样变性肾病综合征中升高最为明显,而在系统性红斑狼疮患者中降低。重症肾病综合征患者的典型特征是激肽释放酶和激肽酶I含量高,同时激肽原含量降低。肾病综合征患者的肾脏损伤还表现为α1 -抗胰蛋白酶和总抗胰蛋白酶活性增加,在I度肾病综合征中达到最大值,在疾病II度时降低。在肾病综合征中,α2 -巨球蛋白的含量在II度肾病综合征时最高,在疾病重症时降低。蛋白酶抑制剂含量的原发性改变和激肽系统成分的高水平被认为决定了血清中激肽系统的激活条件,并损害了伴有全身表现的肾病综合征发病机制。激肽系统成分的高含量显然是由肝脏组织因炎症和大量蛋白尿而增加的合成所决定的;激肽酶I和α2 -巨球蛋白作为高分子量蛋白质,在毛细血管通透性增加时可能会选择性地保留在血液循环中。