Systemic Lupus Erythematosus (SLE) is a complex autoimmune disease. The immunological hallmark of SLE is the production of a range of autoantibodies directed at ubiquitous nuclear components. It is characterized by immune-mediated damage to multiple organ systems with a corresponding diverse array of systemic symptoms. The etiology of SLE is still undetermined, but it is known to involve a complex interaction of genetic and environmental factors 
. SLE has a prevalence of ~40 cases per 100,000 individuals with onset typically occurring in women of childbearing age (F
M ratio 9
. There is a diverse variation in disease prevalence in different ethnic populations with a 3–4 times increased prevalence in African American (AA) 
, and an elevated rate of nephritis relative to European Americans (EA). AA lupus has an earlier age of onset and a clinically more severe phenotype 
. Nephritis is often a severe manifestation of SLE 
and is frequently linked to a poor long-term prognosis with a greater than four-fold increase in mortality 
Current aggressive immunosuppression therapies are effective in controlling renal lupus flares and have improved disease outcomes, but side effects such as infection, malignancy, metabolic disturbances, and infertility make this treatment option unsatisfactory. Potential contributions of microRNA to the pathogenesis and mechanisms of damage to kidneys in SLE-associated nephritis may allow development of more specific, effective, and less toxic therapies. In addition, conventional immunosuppressive drugs for treatment of SLE associated nephritis, such as corticosteroids, cyclophosphamide, and azathioprine, could be used more effectively and with fewer side effects if clinicians could accurately predict SLE-associated nephritis or renal flare and response to treatment 
. The use of unique miRNA expression signatures could be an important and cost-effective means to monitor predisposition to lupus nephritis or its pathogenesis.
Small non-coding RNA molecules (microRNA or miRNA) are a gene expression and protein synthesis modulating mechanism that has been recently identified in several species including humans. These miRNA are single-stranded RNA molecules of about 20–25 nucleotides (nt) encoded by nuclear genes (70–150 nt) and are highly conserved among species. These genes are not translated into proteins but are processed from primary transcripts (called pri-miRNA) to short stem-loop structures called pre-miRNA and finally to functional miRNA. The expression pattern of miRNA varies over time and between tissues. These mature miRNA molecules are partially complementary to one or more mRNA sequences and they function through sequence-specific down-regulation of their target mRNA via mRNA degradation or inhibition of translation 
. In the public miRNA database (miRBase) there are over 700 proposed human miRNA.
MiRNA are now recognized as one of the most highly abundant agents of gene regulation at the post-transcriptional level in higher eukaryotes 
. It is estimated that miRNAs account for 1–5% of expressed genes in the animal genome and about 20–30% of all human mRNA are known to be miRNA targets.
Because miRNA function as managers in gene regulatory networks, they are distinct from other biomarkers because they may have an upstream and potentially pathogenic role in the disease process. Quantitation of miRNA gene expression levels has become an essential step in understanding mechanisms for cellular processes such as cell differentiation, cell proliferation and cell death, and has shown great promise in identifying effective biomarkers that correlate with human diseases 
Although dysregulation of miRNA expression has been characterized mostly in cancer, it has recently been studied in many other diseases. Specifically, miRNA have been proposed as a regulator of immune cell development 
, playing a role in the inflammatory response 
and as a key player in the pathogenesis of neurodegenerative diseases 
. The relationship between SLE and miRNA was first reported by Dai et al who studied the relationship in PBMCs 
and renal biopsies 
obtained from Chinese SLE patients. The role miRNA play in autoimmune diseases is incomplete or only beginning to be characterized especially with regard to miRNA. However, the importance of miRNA on post-transcriptional regulation of gene expression in SLE is emerging with some surprising results. In one relevant example a mouse model of SLE with defects in miRNA regulation of mRNA induced disease. Here miRNA101 suppresses expression of the ICOS (a costimilatory molecule on T cells), which is defective in sanroque model of lupus, leading to stimulation of autoreactive B cells and a lupus-like illness 
. Understanding the role of miRNA in SLE may have important implications for disease pathology.
We evaluated miRNA expression by microarray technology in samples obtained from lupus nephritis patients and unaffected controls. In these samples we identified changes in miRNA expression that correlate with lupus. Five miRNA (hsa-miR-371-5P, hsa-miR-423-5P, hsa-miR-638, hsa-miR-1224-3P and hsa-miR-663) were differentially expressed across different racial groups and in all specimen types tested. Three of these miRNA (hsa-miR-371-5P, hsa-miR-1224-3P and hsa-miR-423-5P) were associated with lupus nephritis and are reported here for the first time. These miRNA may be potential novel biomarkers or may help to elucidate pathogenic mechanisms of lupus nephritis.