[Kinin system components, free kinins and proteinase inhibitors in the edematous fluids of nephrotic syndrome patients].

: Main components of the kinin system, free kinins, total arginine esterase activity content of alpha 1-antitrypsin and alpha 2-macroglobulin fractions were estimated in various edematous fluids (transduates of different localization, pleural exudates of the inflammatory type) of patients with nephrotic syndrome of various etiology. Noninflammatory edematous fluids (interstitial, abdominal and pleural transudates) were found to contain activated kallikrein and prekallikrein from blood plasma; 3-10 ng/ml of free kinins were present in interstitial edematous fluids and 30-60 ng/ml - in abdominal transudate. Kinins of abdominal transudate were identified with bradikinin by chromatographic properties; a single low-molecular form of kininogene was found, its content did not exceed 10% of the substance occurring in blood plasma of the patients. These edematous fluids practically did not exhibit the kininase activity and contained unsignificant amounts of proteinase inhibitors. Pleural exdates of the inflammatory type were distinctly different from transudates in content of the kinin system components. Depending on the higher content of protein (2.5% as compared with 0.3-0.7% in transudates) the exudates contained high-molecular kininogene and kininase I. Relative content of kallikrein in pleural exudates was lower and that of prekallikrein - higher as compared with transudates; acid kininogenases were not observed. Free kinins (30 ng/ml) were found in three samples of pleural exudates out of five samples studied. The inflammatory type of pleural exudates correlated with the high level of alpha 1-antitrypsin. As shown by comparative analysis of protein fractions from edematous fluids and corresponding samples of blood plasma of patients with nephrotic syndrome, diffusion is the main reason, which determines the course of protein transition from inter-into exovasal space, under conditions of increased vascular permeability. Kallikrein activation and extravasal formation of bradikinin were apparently the long-term affecting factors, supporting the state of increased vascular permeability in nephrotic syndrome; they had an aggravating role in pathogenesis of refractory nephrotic edema, nephrotic crises and cutaneous erythema.