What is the pathogenesis of immunoglobulin a nephropathy?
A unifying theory of the pathogenesis has not been fully elucidated. The available data suggest that tissue injury can be initiated by the deposition of abnormally underglycosylated IgA subclass 1 (IgA1) immune complexes in the mesangium.
These complexes somehow trigger mesangial cell activation, which in turn releases proinflammatory cytokines and profibrotic mediators, affecting nearby glomerular structures.
It is also suggested that IgA deposits activate the local complement system.
The higher C3 deposition compared with C1q suggests that the lectin and alternative complement pathways are implicated.
