[Fibrinolytic activity of the urine during chronic glomerulonephritis and amyloidosis].

Correlative interconnections between plasminogen activator (PA) activity (fibrin plate method) and level of urokinase antigen (Ag UAP) and tissue PA antigen (Ag TAP) in urine and blood (ELISA) were studied in 60 patients with chronic glomerulonephritis (CGN) and 38 patients with amyloidosis. The high degree of positive correlation between blood and urine initial PA activity and Ag UAP content was found. This suggests the possible leading role of UAP in formation of the basal fluctuations of fibrinolytic activity in blood and urine.

[Urokinase as a blood and urine plasminogen activator in chronic glomerulonephritis and amyloidosis].

To estimate the individual role of the plasminogen activators (PA) urokinase (u-PA) and tissue (t-PA) in the development of two renal diseases (the nephrotic forms of chronic glomerulonephritis (CGN) and amyloidosis, the baseline plasma and urine levels of u-PA and t-PA antigens, their functional activity (FPAA), and changes in these parameters were determined after protein loading test (0.7 g/kg). In healthy individuals and patients with amyloidosis, the baseline FPAA changes from 0 to the maximum were caused only by the alterations of u-PA levels, in those with CGN, they were induced by the changes in the content of u-PA and t-AP antigens.

[Activators and inhibitors of fibrinolysis in chronic glomerulonephritis and amyloidosis].

Functional activities of plasminogen activators (FPAA) and their inhibitors and plasminogen activators's (PA), antigen level were determined in 31 patients with chronic glomerulonephritis, 23 patients with amyloidosis and 15 healthy persons. High FPAA correlated with favourable prognosis of diseases, elevated PA antigen level and diminished alpha 1-antitrypsin, alpha 2-macroglobulin and antiactivator activities. There were decreased PA antigen level and increased inhibitor's activities in group with zero FPAA.

[The venous occlusion test in assessing the fibrinolytic activity of the vascular endothelium in lupus nephritis patients].

A venous occlusion test was used to evaluate the reserves of the kidneys and that of vascular endothelium fibrinolytic activity (VEFA) in patients with lupus nephritis (LN). Prior to and following venous occlusion functional activity of plasminogen activators in plasma and urine (PAPU), plasma activity of antiactivator (PAAA), urokinase urine activity (UUA) were measured by fibrin plate lysis test in 24 patients with active LN, 6 SLE patients with intact kidneys, 10 healthy subjects. Venous occlusion test revealed normal reserve of plasma activator activity in mild LN and depletion of this reserve in LN patients with nephrotic syndrome and rapidly progressive LN.

[Tissue-type plasminogen activator in patients with lupus nephritis].

ELISA was used to measure tissue plasminogen activator antigen in blood plasma and urine of 42 patients with active lupus nephritis (16 with isolated urinary syndrome, 13 with nephrotic syndrome, 13 with rapidly progressive LN). Control groups consisted of 17 patients with inactive LN and 15 healthy subjects. Inhibition of fibrinolysis in vascular system correlating with the disease severity was found in patients with active LN.

[The clinical importance of determining the von Willebrand factor in patients with lupus nephritis].

Venous occlusion test has found out the reserve of vascular and renal endothelium in excretion of Willebrand factor in patients with inactive lupus nephritis and those with active lupus nephritis with urinary syndrome. In severe active lupus nephritis (lupus nephritis with nephrotic syndrome and rapidly progressive lupus nephritis) it was not recorded. This fact evidences intensity of immune inflammation and coagulation in the kidneys in the above forms of lupus nephritis.

[The functional activity of plasminogen activators in the blood plasma and urine of patients with lupus nephritis].

A fibrin plate technique was employed to study functional activity of plasminogen activators in plasma and urine (FAAP, FAAU), activity of antiactivator in plasma (AAAP), urokinase urine activity (UUA) in 35 lupus nephritis (LN) patients. The latter comprise 3 groups by the disease severity: 22 patients with active LN attended by urinary syndrome (group 1), 7 patients with LN associated with nephrotic syndrome (group 2), 6 patients with rapidly progressing LN (group 3). Control groups included 5 SLE patients with unaffected kidneys and 25 healthy subjects.

[Antistreptococcal antibodies in the blood serum of glomerulonephritis patients].

To study humoral antistreptococcal immunity, 29 patients with acute glomerulonephritis (AGN), 211 patients with chronic glomerulonephritis (CGN) and 30 healthy donors were examined. According to EIA, blood sera of the indicated groups demonstrated antibodies (AB) to structural components of Streptococcus--A-polysaccharide (A-ps) and hyaluronic acid (HA) and to its extracellular products--streptokinase (SK) and streptolysin-O (ASLO). It has been shown that in the blood of AGN patients, the levels of AB to A-ps, SK and ASLO were high.

[The effect of a protein loading test on the fibrinolytic system in patients with chronic glomerulonephritis and amyloidosis].

Investigation of the reserves of the fibrinolytic system with the aid of protein stimulation was carried out in 10 patients with chronic glomerulonephritis and in 10 patients suffering from amyloidosis. All the patients manifested proteinuria exceeding 3.5 g/day and other symptoms of nephrotic syndrome of varying intensity.

[Laser treatment of patients with chronic glomerulonephritis].

Helium-neon laser therapy of patients suffering from mixed and nephrotic glomerulonephritis demonstrated hypotensive, diuretic and fibrinolytic activity boosting clinical effects. The use of the new treatment method seems to be justified, since all the patients given laser therapy manifested pronounced resistance to the pathogenetic therapy carried out previously (glucocorticoids, cytostatics, hypotensive and diuretic drugs). The presence of diverse effects and lack of complications suggest a broader-scale use of laser therapy in nephrology.

[A substrate inhibitor analysis of the urinary excretion of tissue and plasma kallikreins in patients with chronic glomerulonephritis].

The usage of substrate inhibitor analysis made it possible to estimate the levels of excretion of plasma proteinases, including plasma kallikrein in the urinary DValLeuArgpNA (S-2266)- and DProPheArgpNA (S-2302)-amidase activity in patients with latent and nephrotic types of chronic glomerulonephritis (CGN). The soya bean trypsin inhibitor, an inhibitor of plasma kallikrein and other plasma proteinases, such as that of the blood coagulative factors XIa and XIIa, and the high selective plasma kallikrein inhibitor DPhePheArgCH2Cl were used as those differentiating kallikreins of tissue and plasma origin. The S-2266 and S-2302-amidase activity of the urine from healthy subjects was shown to be determined by only tissue (renal) kallikrein.

[Components of kallikrein-kinin system in the urine of patients with glomerulonephritis].

Activities of main components of the kallikrein-kinin system: tissue (renal) and blood plasma kallikreins, kininases I and II, bradykinin-activating activity as well as free kinins, were estimated in urine of patients with latent and nephrotic forms of glomerulonephritis as compared with those parameters in urine of healthy persons. Content of tissue kallikrein was decreased in urine of patients with nephrotic form of glomerulonephritis as distinct from the disease latent form and healthy persons. At the same time, urine of these patients with nephrotic form contained elevated amount of blood plasma kallikrein and other proteinases of blood plasma origin.

[The clinico-morphological characteristics of psoriatic nephropathy].

Based on studying the data obtained during examination of patients with psoriasis combined with the urinary syndrome possible varieties of psoriatic nephropathy, namely chronic glomerulonephritis (CGN) and amyloidosis were distinguished. CGN combined with psoriasis was mainly represented by latent glomerulonephritis (GN) and morphologically, it was mostly represented by the mesangio-proliferative variant, with IgA and C3 being fixed on the basal membrane of the capillaries and in the mesangium. The clinicomorphological feature of that form of psoriatic GN is combination of the signs of both associated CGN and hyperuricemia and IgA-nephritis.

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

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.

[Disorders of purine metabolism as an etiological factor in renal pathology].

Of 3200 patients admitted to the nephrology department within several years, hyperuricemia was detected in 696. Excluding from this number persons with signs of chronic renal insufficiency (146 persons) and patients who were treated by diuretics (89), the frequency of hyperuricemia was 16.2% which exceeded almost 2-fold (9.

[Clinical value of the study of hemostasis in nephrology].

The results of many-year studies on the humoral and platelet links of hemostasis in chronic glomerulonephritis (CGN) and amyloidosis were analyzed with relation to a stage of disease and prognosis of its course. Activation of the blood coagulation system (BCS), platelet hyperaggregation and suppression of the fibrinolytic system were revealed in CGN. Hypercoagulation was most noticeable in patients with active and prognostically unfavorable GGN types correlating with the frequency of local (in the kidney) intravascular coagulation, the frequency of peripheral thromboses and DIC-syndrome.

[Immune complex hyperuricemic nephritis: aspects of its morphology and pathogenesis].

The authors described the results of an immunohistochemical, electron microscopic and morphometric study of the kidney bioptates of 45 patients with latent glomerulonephritis with hyperuricemia, 8 patients with primary gout and 12 patients with latent glomerulonephritis without hyperuricemia. Two possible variants of the involvement of the renal glomerula were revealed against a background of purine metabolism: typical immunocomplex glomerulonephritis and the so called "reactive" mesangial changes. The expression of interstitial changes (by the results of histometric investigation) was maximum in gout, slightly less in latent nephritis with hyperuricemia and minimum in nephritis without hyperuricemia.