<原著>糸球体腎炎における尿中plasminogen activator inhibitor-1の性質
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It is assumed that the persistency of fibrin deposits in the kidney during renal diseases could reflect either a defective release of plasminogen activator (PA) or a local excess of plasminogen activator inhibitor (PAI). In order to clarify the role of fibrinolytic system, PAI-1 antigen, urokinase type-PA (u-PA) antigen, fibrin/fibrinogen degradation product-E (FDP-E) and thrombin-antithrombin-III complex (TAT) were measured in the urine from normal subjects and from the patients with glomerulonephritis including minimal lesion, mesangial proliferative glomerulonephritis and IgA nephropathy. PAI-1 antigen, u-PA antigen and TAT were measured using enzyme immunoassay and FDP-E using latex aggregation method. The values of urinary FDP-E in glomerulonephritis were higher than those from normal subjects and the values of urinary TAT were higher, too. But the values of urinary u-PA antigen in glomerulonephritis were lower than those from normal subjects. The fibrinolytic activity in the urine, which was measured using electrophoretic enzymography, was lower in glomerulonephritis than that in normal subjects. The fibrinolytic activity in the urine was correlated with the u-PA antigen. On the other hand, the values of urinary PAI-1 antigen in minimal lesion, mesangial proliferative glomerulonephritis and IgA nephropathy were 0.10±0.04,0.31±0.09 and 0.26±0.04ng/mg creatinin, respectively, while no PAI-1 antigen was observed in the normal subjects. Also, urinary PAI-1 antigen was correlated with the loss of renal function. The urinary PAI-1 showed the activity which was measured as S-2444 amidolytic activity. The molecular analysis of PAI-1 revealed that 30 KDa and 80 KDa bands by Westen blotting method. This 80 KDa band reacted with anti u-PA IgG by Western blotting method. The lysis zone in the molecular weight of 80 KDa by electrophoretic enzymography disappeared whne it was reacted with anti PAI-1 IgG and anti u-PA IgG. Thus, it is suggested that urinary PAI-1 was in active form, partially made the complex with urinary u-PA antigen. These findings indicate that intraglomerular coagulation and fibrinolytic process participate in the progress of glomerulonephritis which may be modulated by PAI-1.
- 近畿大学の論文
- 1991-06-25
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