<unk>  often occurs as a result of glomerular injury, though can be idiopathic.<unk>  has been associated with disease processes such as: IgA nephropathy, IgM nephropathy, systemic lupus erythematous, Alport's syndrome, resolving post-infectious glomerulonephritis, and complement nephropathy, such as C1Q nephropathy. IgA nephropathy is the most common cause of<unk> . It is thought abnormally glycosylated IgA form polymers and deposit in the mesangium. Subsequently, IgA immune complexes bind to IgA receptors on mesangial cells and induce injury to mesangial cells through release of cytokines and growth factors that promote infiltration of leukocytes, mesangial cell proliferation, and mesangial matrix expansion. In the context of resolving post-infectious glomerulonephritis,<unk>  can be seen after an infection with a nephritogenic strain of group A streptococci. Pathogenesis of post-streptococcal glomerulonephritis includes injury to the glomerulus by immune complexes (IgG) passively trapped in the glomerulus, which leads to an inflammatory response from recruited immune cells, cytokines, chemical mediators, and complement and coagulation cascade activation. The inflammatory response includes endothelial and mesangial cell proliferation.<unk>  of Lupus nephritis, Class II is also noted by mesangial hypercellularity and matrix expansion. Microscopic haematuria with or without proteinuria may be seen in Class II Lupus nephritis. Hypertension, nephrotic syndrome, and acute kidney injury are very rare at this stage. Idiopathic<unk>  is less established in the literature. Idiopathic<unk>  does not involve the deposition of either IgA or IgG immune complexes, though there can be focal or diffuse IgM deposits in the mesangium. The relationship of IgM and<unk>  is hypothesized to involve either formed or deposited IgM complexes in the mesangium leading to T-cell mediated inflammatory response, mesangial proliferation, and glomerular injury or, as a result of mesangial proliferation, decreased clearance of monocytic IgM complexes.
Mesangial proliferative glomerulonephritis
Membranous glomerulonephritis
Minimal mesangial glomerulonephritis
Membranoproliferative glomerulonephritis
Focal proliferative nephritis
Transplant glomerulopathy
Diffuse proliferative nephritis
Rapidly progressive glomerulonephritis