الفهرس 
INTRODUCTIONOnly 14 pages are availabe for public view
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Abstract
Systemic lupus erythematosus (SLE) is a multisystem autoimmune disorder with a broad spectrum of clinical presentations affecting almost all tissues and organs. Its presentation and course are highly variable, ranging from indolent to fulminant. The incidence was nearly tripled in the past 40 years due to improved detection of mild disease. The exact cause of SLE is unclear, but several factors have been associated with the disease including genetic, hormonal and environmental factors. Interaction among this factors leads to loss of immune tolerance, increased antigenic load, and the production of pathogenic autoantibodies.
Lupus nephritis (LN) is an inflammation of the kidney that is caused by immune complexes deposition leading to local complement activation, subsequent cytokines and chemokines secretion, and cell injury. It is one of the most serious complications of SLE and the major predictor of poor prognosis. It was found that about 50–60% of SLE patients develop nephritis during the first 10 years of the disease.
It has been found that, the diagnosis of LN could be missed in 13 % of the SLE patients with proteinuria less than 0.5 g/day and progress to ESRD. Therefore, selection of SLE patients at high risk for developing LN to be subjected to renal biopsy is of great importance to help in early detection and treatment reducing its morbidity and mortality.
Familial clustering of LN has been observed, suggesting that genetic factors contribute not only to the risk of SLE but also to LN. Tumor necrosis factor alpha induced protein 3- interacting protein1 (TNIP1) intronic SNP (rs7708392) had been reported in a genome-wide association study (GWAS) to be associated with SLE in the European, and African American. However, the effect of TNIP1 (rs7708392) polymorphism on susceptibility to LN is still under investigation.