[1] The increase in the number of mesangial cells can be diffuse or local and immunoglobulin and/or complement deposition can also occur.

[2] Treatment is often consistent with the histologic pattern of and/or disease process contributing to mesangial proliferative glomerulonephritis, and usually involves some form of immunosuppressant.

[3] In the context of resolving post-infectious glomerulonephritis, MesPGN can be seen after an infection with a nephritogenic strain of group A streptococci.

[4] 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.

[2] Preceding infection was not as readily identified in patients presenting with either asymptomatic proteinuria or nephrotic syndrome.

However, it has been shown patients presenting with nephrotic syndrome have some histo- and clinic-pathologic similarities to minimal change disease.

[2] Presentation of nephrotic syndrome in the context of mesangial proliferative glomerulonephritis have been treated with immunosuppressants, such as steroids and cyclophosphamide.