Abstract

Systemic lupus erythematosus (SLE) is the classical systemic autoimmune disease with heterogeneous manifestations and unpredictable behaviour in which almost 70% may have a relapsing-remitting course, while 30% are divided equally between prolonged remission and persistently active disease [ [1] Tselios K. Gladman D.D. Touma Z. Su J. Anderson N. Urowitz M.B. Disease course patterns in systemic lupus erythematosus. Lupus. 2019; 28 ([Internet]JanAvailable from:): 114-122http://www.ncbi.nlm.nih.gov/pubmed/30526328 Crossref PubMed Scopus (28) Google Scholar ]. According to the mosaic of autoimmunity [ [2] Shoenfeld Y. Isenberg D.A. The mosaic of autoimmunity. Immunol Today. 1989; 10 ([Internet]AprAvailable from:): 123-126http://www.ncbi.nlm.nih.gov/pubmed/2665774 Abstract Full Text PDF PubMed Scopus (157) Google Scholar ], immune responses (innate and adaptative), as well as interaction of genes with environmental factors (ultraviolet radiation, smoking and drugs, such as, procainamide, hydralazine and anti-tumour necrosis factor agents) lead to numerous immunologic abnormalities that culminate in persistent immune responses against autologous nucleic acids. In this scenario, lupus nephritis (LN), the most frequent severe complication appears in 35% to 50% of patients in the first ten years of disease and contributes as a major cause for morbidity, rising medical expenses and mortality in SLE.

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