As the patient's skin and liver disease can be detected IgA deposition,
suggesting systemic disease. Since the mesangial area and capillary can granular
IgA and C3 deposition, suggesting that the pathogenesis of immune complexes.
Current research revolves around the ability of antigen through the mucosa,
mucosal barrier existence of defects; IgA structure is flawed and whether there
are defects in immune function and other aspects. Early studies suggest the
disease had deposited mucosal IgA may be derived. However, recent studies using
highly specific technical, confirmed that the disease is deposited IgA1, mainly
the system derived mainly produced by the bone marrow and lymphatic system;
mucosa-derived IgA2 is mainly seen Hepatogenic kidney glomerulosclerosis in IgA
deposition. In patients with this disease can also be seen circulating total
IgA1 and IgA1-containing immune complexes increased, resulting in IgA1 of bone
marrow plasma cells increased and the formation of polymer-based. In the renal
tissue of the disease can be found in the presence of J chain, it prompts IgA is
deposited polymer; and secretion block is very rare. Nevertheless, the available
information is not yet finalized origin of the disease IgA deposits.
A large number of antigens, including a variety of viruses and a variety of
food antigens can be detected in mesangial area of the patient's disease, and is
often accompanied by IgA1 deposition. These antigens also is IgA1. Since these
antibodies can also be present in the normal cycle, there is no specific or said
antigenic characteristic.
There is evidence to suggest the presence of immune dysregulation disease.
This disease circulating immune complexes containing IgA1 found how cohesive
IgA1 rheumatoid factor; anti-α heavy chain Fab fragment of IgG antibodies
increase and decrease IgM antibodies. Interestingly HIV infection there is a
similar pattern of anti-immunoglobulin, renal IgA deposition does not occur.
This proves that only the existence of these circulating autoantibodies, not
because mesangial IgA deposition. Also present also found two kinds of
anti-endothelial cell autoantibodies (an IgG). The disease often C3 deposition
in renal tissue, suggesting that activation of the alternative complement
pathway. However, IgA itself has no ability to activate complement, IgA immune
complexes although complement pathway can be activated, but it combines the
ability to complement and C3b weak. Generally considered to occur in the kidneys
of complement activation and the formation of membrane attack complex, the need
for IgG-IgA complexes, but this disease in renal tissue IgA and C3 deposition
have no IgG or IgM deposition is very common. Thus, complement activation
mechanism of the disease is unknown. Cellular immunity is also involved in the
pathogenesis. The disease has been found to have T helper cells (CD4) and T
suppressor cells increased (CD8) decrease; with IgM synthesis to convert
synthesis Ta4 IgA cells increased the frequency of alleles relating Sa1
increases; cause IgA isotype switching of TGFβ, IL-4 produced IgA promote the
differentiation of B lymphocytes and IL-5 mediated IgA production formation were
increased. Although T cells and B cells are involved in the increase in IgA
synthesis process, but not because of increased synthesis of IgA mesangial
deposits of IgA, because IgA deposition in IgA organized a rare multiple myeloma
patients. Therefore, the structure - Immunology / physicochemical only exception
may be the cause of mesangial IgA deposition.
The disease patient serum and mesangial can be detected in anti-bovine serum
albumin genotypes polyclonal antibody titer associated with hematuria. Recently,
someone with IgA and glomerular renal cortex obtained from a patient got five
kinds of monoclonal antibodies against gene, they serum or plasma cell response
is poor and the patient, regardless of their kidney tissue has a high response
rate, suggesting that the kidney IgA deposition with these polyclonal antibodies
abnormal nature. In addition, patients with this disease were found to have
defects β1,3- galactosyltransferase changed IgA1 or complexes containing IgA1
clearance, resulting in mesangial IgA1 deposition.
In summary, the deposition of antigen, with or without a cell-mediated immune
response, IgA complex formation rate and have IgAFc receptors mesangial cells or
neutrophils involved in the scavenging efficiency of the entire pathogenesis,
and Cytokines and growth factors are mainly involved in the mesangial
proliferation and hardening mechanisms.
If you still have problems, you can contact us by email:
kidneyhospitalabroad@hotmail.com.
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