Mechanism of antinephritic effect of proteinase inhibitors in experimental anti-GBM glomerulopathy.

We have previously documented amelioration of rat autologous anti-GBM nephritis with the antiproteolytic drugs epsilon-aminocaproic acid (EACA) and aprotinin, given from the day of induction or later in the course of disease. In the present study we investigated potential mechanisms of this effect by assessing interactions of the drugs with proteinase-dependent generation of superoxide anion in glomeruli, and their influence on both GBM degradation in vitro and activity of glomerular proteolytic enzymes. Release of O2- by enzymatically disrupted glomeruli, isolated from nephritic control or EACA/aprotinin-treated rats, was measured with the ferricytochrome reduction method and its activity was correlated with proteinuria and glomerular cellularity at the early phase of the disease.

Different erythrocyte and platelet surface electric charge in various types of glomerulonephritis.

Background: Some preliminary observations suggest that predisposition to a particular type of glomerulonephritis (GN) may be connected with the genetically determined charge of the glomerular capillary wall. A correlation between erythrocyte surface and the glomerular capillary wall charges has also been observed. The purpose of this study was to verify and extend previous investigations.

Effect of antiproteolytic drugs: epsilon-aminocaproic acid (EACA) and aprotinin on experimental anti-GBM nephritis.

Background: Given the evidence accrued by other authors on beneficial effect of protease inhibitors on experimental immune nephritis, and following our preliminary report on abrogation of immune glomerulopathy in the rat by antifibrinolytic and antiproteolytic drug, epsilon-aminocaproic acid (EACA), we investigated the effect of this drug on the rat autologous anti-GBM nephritis. Along with the EACA we evaluated another protease inhibitor, aprotinin, an antagonist of serine proteases.

Methods: EACA (0.