[State of the kinin system and level of serum proteinase inhibitors in latent nephritis and the nephrotic syndrome of different etiology].
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.
D001120:Arginine; D001555:Benzene Derivatives; D004950:Esterases / Q000097:blood; D005921:Glomerulonephritis / Q000097:blood* / Q000201:enzymology; D006801:Humans; D007610:Kallikreins / Q000097:blood; D007704:Kininogens / Q000097:blood; D007705:Kinins / Q000097:blood*; D001121:Lysine Carboxypeptidase / Q000097:blood; D009404:Nephrotic Syndrome / Q000097:blood* / Q000201:enzymology; D014361:Trypsin Inhibitors / Q000097:blood; D000515:alpha 1-Antitrypsin / Q000032:analysis; D000511:alpha-Macroglobulins / Q000032:analysis
D001555:Benzene Derivatives; D007704:Kininogens; D007705:Kinins; D014361:Trypsin Inhibitors; D000515:alpha 1-Antitrypsin; D000511:alpha-Macroglobulins; D001120:Arginine; D004950:Esterases; D001121:Lysine Carboxypeptidase; D007610:Kallikreins
Sostoianie kininovoĭ sistemy i uroven' ingibitorov proteinaz syvorotki krovi pri latentnom nefrite i nefroticheskom sindrome razlichnoĭ étiologii.