The Membranoproliferative glomerulonephritis pathogenesis

MPGN pathogenesis is not clear that related to the immunological mechanisms. 50% to 60% of MPGN serum complement C3, C1q and C4 lower, suggesting that the alternative pathway and classical pathway are activated and lead to complement lower blood.Accompanied by a mild increase in immune complexes and cryoglobulinemia, and immunoglobulin and complement deposition in glomeruli. However, the relationship between complement abnormalities and disease, the role of immune complexes remains to be further explored.
According to the extent of a variety of immune complex deposition in the form of glomerular basement membrane and mesangial area and deposition of different MPGN divided into three types.
Main complex deposition within the subcutaneous type Ⅰ mesangial area. Type Ⅰ and viral, bacterial and parasitic infections and some immune complex diseases (such as the lack of genetic complement, SLE, mixed cryoglobulinemia, SBE in shunt nephritis, lymphoma, schistosomiasis), but often as idiopathic. Hypocomplementemia I MPGN patients, 33 percent to 50 percent, 25 percent to 30 percent in patients with Clq, C4 and C5 lower, 15% to 20% of patients with B-factor decreased.
Type II is known as autoimmune diseases, can be observed in the electron microscope was uniform ribbon deposition along the basement membrane laminin layer, this type is also known as dense deposit disease (DDD), also often accompanied by subepithelial hump-like sediment deposition. PAS staining is sometimes visible banded deep dye on the capillary loop. Type Ⅱ with streptococcal infection, Streptococcus kidney antigen cross-reactive antibody-mediated can cause kidney damage. Type Ⅱ often complicated by low plasma C3 level, as part of the blood in patients with complement activator, an autoantibody, also known as induced nephritis factor C3 nephritis factor, the direct anti-C3bBb, change the C3 bypass conversion by converting enzyme combination to prevent some of the normal inhibitory factor, such as the role of factor H, an increase of complement activation and consumption. C3 nephritis factor is more common in type I and type II MPGN, especially in the more common type Ⅱ. Part Lipodystrophy. MPGN II-type basement membrane damage and, if the dense sediment deposition in the basement membrane, these sediments can activate complement, complement some special substances, such as ribozyme activation is usually activate the alternative pathway, so that C3 nephritis factor secondary continues to increase, which led to the decline of the blood complement C3. Type Ⅱ MPGN in. 70% of patients C3 and factor B reduced.
III-type endothelial, mesangial and subepithelial have sediment deposition. Type III and type Ⅰ difference is that the subepithelial deposition.
Accompanied by the migration of time, the MPGN The pathological changes of more than from hyperplasia to a significant hardening. Subtypes, the focal type MPGN lesions may shift behavior filled with classic MPGN. Some children or young people, began to diffuse MPGN subtype of multi-leaf type, shift behavior focally or complete remission.