Characteristics of immunoglobulin A nephropathy with mesangial immunoglobulin G and immunoglobulin M deposition

Abstract

The presence of other Ig classes, besides IgA deposits, was found to be associated with glomerular obsolescence and tuft adhesions, however, without any effect on renal survival in IgAN.

Spontaneous glomerular mesangial lesions in common marmoset monkeys (Callithrix jacchus): a benign non‐progressive glomerulopathy

“…Concurrently, electron‐dense mesangial deposits were observed in the majority of marmoset kidneys by electron microscopy. Similar deposits in human kidneys are characteristically seen in immune complex nephropathies such as systemic lupus erythematosis and IgA nephropathy , although the presence of IgM deposits does not seem to confer any prognostic significance. Immunoglobulin deposition may also occur in otherwise normal human kidneys .…”

Nefropatia por IgA: análise histológica e correlação clínico-morfológica em pacientes do Estado de Minas Gerais

“…Em nosso estudo, a codeposição IgA+IgM foi mais frequente que IgA+IgG. Moriyama et al 39 demonstraram que a concomitância de deposição de IgG e IgM estaria associada à esclerose glomerular e à adesão de tufos capilares, porém tal patogênese e achados histopatológicos seriam ainda incertos e não exerceriam influência na função renal a longo prazo. A porcentagem de casos com deposição de C3 confirma a literatura prévia que evidencia tal fração do complemento em mais de 90% das biópsias.…”

Clinical characteristics of IgA nephropathy associated with low complement 4 levels

“…The gradually accumulated renal IgM deposition is associated with heavy proteinuria, 42 crescents formation, 43,44 increased mesangial matrix as well as mesangial and perimesangial electron-dense deposits 45 leading to a poor outcome in IgAN. 46 We presumed that the lectin pathway may not be activated sufficiently under the condition of C4 deficiency, which protect the glomeruli from the initial injury at the time of renal biopsy. However, the gradually accumulated IgM and immune-complex deposition that cannot be removed by C4 may result in chronic glomeruli injury via promoting PDGF, TGF-b, and TLR-4 leading to a poor outcome.…”