The pathophysiology of this disorder is consistent with an immune-complex-mediated mechanism, a type III hypersensitivity reaction. This disorder produces proteins that have different antigenic determinants, which in turn have an affinity for sites in the glomerulus. As soon as binding occurs to the glomerulus, via interaction with properdin, the complement is activated. Complement fixation causes the generation of additional inflammatory mediators. Complement activation is very important in<unk> . Apparently immunoglobulin (Ig)-binding proteins bind C4BP. Complement regulatory proteins (FH and FHL-1), may be removed by SpeB, and therefore restrain FH and FHL-1 recruitment in the process of infection.
Acute proliferative glomerulonephritis
Shunt nephritis
Diffuse proliferative nephritis
Focal proliferative nephritis
IgA nephropathy
Rapidly progressive glomerulonephritis
Lupus nephritis
Membranous glomerulonephritis