Mesangial proliferative glomerulonephritis is caused by what

(A) causes
Membranoproliferative glomerulonephritis according to their clinical and laboratorycharacteristics are divided into primary and secondary glomerular disease.
Primary membranoproliferative glomerulonephritis of unknown etiology, is generally believed that type Ⅰ immune complex disease; type II immune complexes andautoantibodies in disease, may be related to heredity.
Secondary mixed cryoglobulinemia, membranoproliferative glomerulonephritis, there arethree kinds of subtypes. Type Ⅰ cryoglobulinemia monoclonal peaks globulin, usually amyeloma protein. Type Ⅱ usually a combination of IgG monoclonal peak of IgM globulin, also known as anti-IgG rheumatoid factor, and type Ⅲ is a multi-strain peakimmunoglobulin. Type Ⅱ and Ⅲ cryoglobulinemia prone to kidney damage. Itspathological features proliferated mesangial cells, white blood cells especiallymononuclear cell infiltration, glomerular basement membrane thickening of the double-track phenomenon. About 1/3 cases of small and medium-sized arteritis, capillarymicrothrombosis. The etiology and pathogenesis of MPGN is not very clear. Type ⅠMPGN immune complex disease, repeatedly sustained by the relatively large insolubleimmune complex deposition. Patients with type II MPGN serum immune complexes,cryoglobulin, complement abnormalities, sustained reductions in serum C3. Promptimmune complexes in the type of MPGN II. Can be detected in patients with type II MPGNserum C3 nephritis factor (C3NeF), C3NeF, C3bBb converting enzyme autoantibodies,C3bBb role to strengthen, leading to sustained activation of the complement bypass, resulting in the degeneration of sustained hypocomplementemia and basement membrane. Complement metabolic disorder as the central link.
In addition, the type II MPGN kidney transplantation often relapse may be due to materialdeposition can cause abnormal glycoproteins in the basement membrane nephritis inserum.
The disease may be related to inheritance, type II MPGN often in patients with HLA-B7.Most of type Ⅰ MPGN patients with a special B-cell alloantigen.