Pathogenesis of membranous glomerulonephritis

Pathogenesis of membranous glomerulonephritis

1 potential pathogenic antigens

Although some scholars have reported finding a series of antigens including DNA, thyroglobulin, tumor associated antigen, renal tubular epithelial antigen and hepatitis B virus in patients with membranous nephropathy glomerular subepithelial deposition in the compound, but only the protein will not cause disease. At present, it is not clear that the antigens and antibodies that cause the immune complex deposition in the glomerular basement membrane.

2 subepithelial immune complex formation

Protein Dioxon and Germuth (2.5mg/d) application of small dose of daily injections caused chronic serum sickness in rabbits, the renal lesions similar membranous nephropathy, deposition of immune complexes in the subepithelial immune complex molecules smaller found only in circulation. On the contrary, if the rabbits received different doses and methods of the opposite sex protein, there would be a larger particle of immune complexes, the deposition of which is not the upper part of the skin. Germuth stressed that the immune complex membranous nephropathy in circulation should have small molecular weight, with two large amounts of negative charge, but the two points in the real body and is not easy to be had at the same time, the reliability of the circulating immune complex theory still have doubts.

The theory of the lesion can react by non natural antigen antibody and circulating a glomerular caused, the latter is due to some biochemical properties and electrostatic affinity of basement membrane and pre implanted to the in situ formation of glomerular immune complexes, and glomerular injury.

This is the formation of the in situ immune complex by the reaction of the local antigen components of the glomerulus and the circulating antibody. This is a generally accepted theory since 1980s.

3 complement mediated

The membrane attack complex (MAC) can insert the phospholipid bilayer structure of the glomerular epithelial cell membrane, cause the damage of cell membrane structure, affect the synthesis and repair of the glomerular basement membrane, and change the capillary permeability. Immunoelectron microscopy confirmed that the membrane attack complex can be epithelial cells from the basolateral membrane of renal capsule is transferred to the side, and after exocytosis discharged into the urine, the initial illness or immune activity in membranous nephropathy urine excretion increased the membrane attack complex. MAC can also activate the glomerular epithelial cells, so that the local release of inflammatory mediators and oxygen free radicals directly acting on the basement membrane. A large number of oxygen free radical release caused by lipid oxidation, collagen degradation of glomerular epithelial cells and basement membrane and increase the permeability of base membrane on protein, which causes proteinuria, plus probucol (Bing Dingfen) (Probucol) proteinuria reduction 85% of this antioxidant.

The study found that glomerular epithelial cell functions, such as glomerular epithelial cell membrane with shrinkage, against 4.67kPa (35mmHg) of the transmembrane hydrostatic pressure of epithelial cells is an important component of the glomerular filtration barrier; integration of epithelial cells and cell adhesion molecules in the alpha 3 beta 1 reaction; release a variety of cytokines and inflammatory mediators including:

(1)Bioactive esters: PGE2 four,, TXA2, etc., as well as lipoxygenase products 12- hydroxy acid (12-HETE).

(2)Tissue inhibitors of metalloproteinases (MMP) -9 and some matrix metalloproteinase (TIMP).

(3)Fibrinolytic factor: tissue type and urokinase type plasminogen activator and inhibitor.

(4)Transforming growth factor (TGF), platelet growth factor (PDGF) and epidermal growth factor (EGF).

(5)Cytokines associated with inflammation, immune recognition, chemotaxis, such as interleukins.

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