Autoantibodies lupus nephritis

Hogan, S. L. et al., Silica exposure in anti-neutrophil cytoplasmic autoantibody-associated glomerulonephritis and lupus nephritis, J. Am. Soc. Nephrol., 12, 134, 2001. 

Anti-dsDNA antibodies are both specific and pathogenic to SLE. As mentioned previously, these autoantibodies are produced by an antigen-driven mechanism. They are organ-specific, especially kidney. We will discuss the close relationship between anti-dsDNA and lupus nephritis and the proposed mechanism by which anti-dsDNA leads to lupus nephritis. 

All of these therapies are under development. The treatment of SLE is still a challenging task for the physician. The importance of the effective treatment of lupus nephritis is reflected by the results of mass urinary screening for school children in Taiwan The most important secondary glomerulonephritis discovered by the screening is SLE with lupus nephritis (L19). In order to achieve a better prognosis, physicians need to be familiar with the effects of autoantibodies, diagnose SLE early, and treat it with appropriate methods. 

Ml. Madaio, M. P., The role of autoantibodies in the pathogenesis of lupus nephritis. Semin. Nephrol. 

Siegert, C., Daha, M., Westedt, M. L., van der Voort, E., and Breedveld, F., IgG autoantibodies against Clq are correlated with nephritis, hypocomplementemia, and dsDNA antibodies in systemic lupus erythematosus. J. Rheum. 18, 230-234 (1991). 

It is notable that cadmium as well as mercury and gold can initiate or aggravate autoimmune manifestations in normal or autoimmune-prone animals, respectively. It would seem likely that these heavy metals have the same effects on humans, presumably by a similar mechanism. Autoimmune manifestations induced by heavy metals include lupus-type nephritis, autoimmune haemolytic anaemia, and skin diseases, such as pemphigus and scleroderma-like lesion. Some manifestations of immune-mediated nephritis and elevation of circulating autoantibodies have been noted in case-studies of persons exposed to gold and cadmium as well as mercury (Ohsawa, 1993 Bigazzi, 1994, 1999). 

Similar to mercury and cadmium, lead has the potential to accelerate expression of autoimmune predisposition lead accelerated the death of male, but not female, NZB/NZW mice due to spontaneously developing autoantibodies and glomerulonephritis (Lawrence et al., 1987) and exacerbated the susceptibility of NZ mixed strains to develop lupus-type nephritis (Hudson et al., 2003). This potential contribution of lead to autoimmune disease remains a valid concern. 

Associations of several autoimmune diseases with atherosclerosis have been observed and a role for LDL oxidation especially in systemic lupus erythematosus (SLE) has been suggested (Frostegard et al. 2005 Hayem et al. 2001 Svenungsson et al. 2001). OxLDL forms immune complexes with p2GPI, which can be detected in the plasma of patients. OxLDL/p2GPI complexes have been demonstrated in patients with syphilis, infectious endocarditis, diabetes melli-tus, antiphospholipid syndrome and chronic nephritis, indicating that oxidation of LDL and the formation of complexes with p2GPI is not restricted to SLE. It is hypothesized that these autoantibodies accelerate the development of atherosclerosis in autoimmune patients. 

Systemic lupus erythematosus is an autoimmune disease that causes affectation not only of the skin but also of other organs, resulting in photosensitive skin eruptions, arthritis, serositis, nephritis, and hematologic abnormalities. It is produced by circulating autoantibodies, immune complexes, and complement deposition that leads to cell and tissue injury [145]. In several open clinical trials, patients with systemic lupus erythematosus have been treated with ECP using 8-MOP, showing a significant response to the treatment, with no or minor side effects [146]. 

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