Pathogenesis of Henoch Schonlein purpura nephritis in childr

Pathogenesis of Henoch Schonlein purpura nephritis in childr

The basic pathological changes of Henoch Schonlein purpura nephritis are glomerular mesangial proliferation and mesangial IgA deposition

, pathological changes vary greatly.

Henoch Schonlein purpura nephritis in children

Henoch Schonlein purpura nephritis in children

The significant feature of IgA in the Henoch Schonlein purpura nephritis is the granular IgA deposition in the mesangial area, which is similar to that of IgA nephropathy

There is an important role in the disease, and even some people think that they are essentially the same disease. Further studies have found that there is a striking consistency between the two mechanisms

, such as elevated serum IgA, monomer and poly IgA, elevated -IgAl, both of the serum circulating IgA immune complexes

All of the glomeruli were mainly composed of poly IgA1 and had J chain deposition. Both of them had C4a and C4b subtypes, and all had IgAlO type glycosylation abnormality, and so on. China

In the University of science and technology, Tongji Hospital Affiliated to Tongji Medical College conducted a comparative study found that in 120 cases of allergic purpura nephritis and 31 cases of IgA nephropathy

Henoch Schonlein purpura nephritis () had 6.3% IgG with a linear deposition along the glomerular capillary wall and a positive anti glomerular basement membrane antibody, and was not IgA

The main sediment, therefore, is at least a healthy search in a part of Henoch Schonlein purpura nephritis, and its pathogenesis is significantly different from that of IgA nephropathy. Allergic purple

Kidney damage by complement nephritis play an important role in the activation of complement may be achieved through the alternative pathway: IgA has no ability to activate C1q and

It can directly activate C3, and the C3 and C3PA are confirmed in the glomerular mesangial region, but there is no C1q and C4. The lack of the patient is susceptible to the activation of the complement system

A series of inflammatory mediators lead to local inflammatory changes, followed by coagulation and fibrinolysis disorders, small vessel thrombosis and fibrin

Deposition, leading to glomerular injury.

 

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