Critical Analysis of Suggested Mechanisms of Pathogenesis of the Post streptococcal Glomerulonephritis

Abstract

Acute glomerulonephritis is a severe kidney disease that develops as a result of streptococcal skin and upper respiratory infections most commonly caused by M serotypes of the group A b-hemolytic streptococci (GAS). Most often this process is acute, but can have a tendency to the chronisation which often leads to renal dysfunction with the development of secondary renal hypertension that can be fatal. In spite of the numerous clinical and experimental studies data on the pathogenesis of the post streptococcal glomerulonephritis remain limited and come to several approaches:

1) cross-reactive antigenes of GAS and renal tissue;

2) streptokinase of GAS, some allele variants of which can transform plasmin to plasminogen that leads to complement activation and deposition of the C3 complement fraction in glomeruli;

3) cysteine protease or pyrogenic exotoxin B of GAS that bind plasmin and laminin as well as break up fibronectin and vitronectin;

4) increased serum concentration of different highly active oxygen-containing substances;

5) IgG Fc-receptors of GAS. All of above hypothesis have arguments "pro" and "contra", so, further experimental studies is necessary for more detail understanding of pathogenesis of the post streptococcal glomerulonephritis.