Lupus nephritis etiology

The etiology of SLE and lupus nephritis (LN) is not yet fully defined. Mainly due to a number of factors, such as genetic, viral infection, immune abnormalities, sunlight or ultraviolet radiation, some drugs induced and estrogen and other autoimmune inflammatory diseases. Its induced kidney disease (ie, LN) is typical of autoimmune complex nephritis.
     1. immune genetic defects
SLE and genetic factors related to the incidence of the family as high as 3% to 12%, there is a clear tendency to gather the family. In the SLE patients with a wide range of studies found that SLE closely related genes found in some of the HLA gene sites, especially the HLA DR region, HLA phenotype was polymorphic. Studies have shown that haploid HLA B8 / DR2 in the population is more likely to produce hypersensitivity to cellular and humoral reactions; this may be due to the presence of HLA-encoded polymorphisms in T and B lymphocytes and antigens For T inhibition of cell dysfunction, autoantibodies and globulin increased. It is now believed that the SLE susceptibility gene is a gene of different structures of T cell antigen receptors. Recent studies have found that some of the T cell B chain polypeptide structure and HLA DR in the same individual at the same time, improve the possibility of the pathogenesis of SLE. In addition, SLE also has a variety of complement defects, such as C2, C1q, C1r, C1s, C4, C5, C8 and Bf, TNF, C1 esterase inhibitor deficiency. These complement components or genetic defects, can affect the traditional complement activation pathway, increase the body's sensitivity to infection and other factors and SLE susceptibility related.

2. external environmental factors
Induced or aggravated SLE many external factors, including chronic infection, drugs, physical factors, emotional stimuli, living environment and so are more important.
Commonly known as chronic viral infection, under the electron microscope found in patients with SLE patients with tube-like inclusion bodies, and vice mucin nuclear protein and core tubular structure similar, but further study that this is a cell damage non-specific which performed. It was also found in SLE patients with glomerular endothelial cell plasma, vascular endothelial cells, lesions were found similar inclusion body material. But the inclusion of body-like substances from the organization has not been able to separate the virus, so the relationship between these substances and virus infection to be confirmed. In SLE patients, there are a variety of high titer antiviral antibodies, such as anti-measles, anti-rubella, anti-parainfluenza, anti-EB virus, anti-epidemic mumps, anti-stick virus and other antibodies. In patients with serum ds-DNA, dsRNA and RNA-DNA and other retrovirus antibodies. It has also been suggested that the incidence of SLE and C-type RNA virus is closely related. In general, there are many indications that viral infection may be one of the causes of SLE, but has not yet confirmed the virus infection and SLE patients with immune regulation abnormalities and autoimmune. In addition, some people think that the incidence of SLE and tuberculosis or streptococcal infection.

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