What Cause IgA Nephropathy

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.


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The Cause of IgA Nephropathy

IgA nephritis main causes are the following:

(1) immune disorders
The presence of IgA rheumatoid factor in 30% of iga nephritis patients, indicating the source of the non-mucosal immunoglobulin. Check in peripheral blood lymphocytes of patients found, iga nephritis patients with IgA specific helper T cells increased and IgA-specific suppressor T cells decreased, OKT4 / OKT8 ratio increases. However, this change is unclear T cell subsets are IgA reason for the increase is the result.

(2) abnormal mucosal immunity
Pathological iga nephritis suggesting basement membrane containing IgA deposition J chain, indicating that may be secreted IgA plasma cells. Some iga nephritis patients with epithelial cells containing secretory IgA intestinal or respiratory symptoms. In addition, in some iga nephritis patients were found to have anti-diet antigens (such as gliadin, bovine serum albumin) and against respiratory pathogens (such as cytomegalovirus, adenovirus, hepatitis virus) IgA antibodies. This further illustrate the intrinsic link between iga nephritis and mucosal immunity. In recent years, the use of the mucosal immune method successfully established animal model iga nephritis, but supports this theory.


Is described above for the relevant IgA nephritis cause, you are aware of this, and if you still want to know more about kidney disease, welcome to consult our doctors or you can send email: kidneyhospitalabroad@hotmail.com.