ArticleMolecular biology reports2010
Anti-alpha-actinin antibodies in relation to new-onset systemic lupus erythematosus and lupus nephritis.
Article in Molecular biology reports, 2010. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 7 papers.
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Who cites it
7 citing papers in PubMed, 9 citations in OpenAlex.
- Diagnostic test accuracy of novel biomarkers for lupus nephritis-An overview of systematic reviews.PloS one · 2022Review
- Patients with Proliferative Lupus Nephritis Have Autoantibodies That React to Moesin and Demonstrate Increased Glomerular Moesin Expression.Journal of clinical medicine · 2021Article
- Utilization of Biomarkers in Lupus Nephritis.Advances in chronic kidney disease · 2019Review
- Precision medicine in lupus nephritis: can biomarkers get us there?Translational research : the journal of laboratory and clinical medicine · 2018Review
- Serum alpha-actinin antibody status in systemic lupus erythematosus and its potential in the diagnosis of lupus nephritis.Caspian journal of internal medicine · 2016Article
- Hypomethylation of interleukin 6 correlates with renal involvement in systemic lupus erythematosus.Central-European journal of immunology · 2014Article
- Glomerular antibodies in lupus nephritis.Clinical reviews in allergy & immunology · 2011Review
Corrections and comments
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Authors and funding
6 authors at 2 institutions in 1 country.
Funding
No grant is acknowledged in the PubMed record.
Abstract
The aim of this study is to investigate the role of anti-alpha-actinin antibodies in patients with new-onset systemic lupus erythematosus (SLE). Thirty-six patients with SLE, 16 of whom had lupus nephritis (LN), and 53 healthy controls were included. The clinical and laboratory parameters of patients were collected from medical records or by questionnaire. Serum anti-alpha-actinin Abs was measured by competitive enzyme linked immunosorbent assay (ELISA). Our results show that the OD value of serum anti-alpha-actinin Abs in SLE patients was significantly lower than that in normal controls (1.212 +/- 0.244 vs. 1.364 +/- 0.202, P = 0.002); seven of 36 SLE patients were seropositive for anti-alpha-actinin Abs, which was significantly higher than in normal controls (19.4 vs. 3.8%, P = 0.028). There were no significant differences of clinical parameters between the anti-alpha-actinin Abs-positive patients and the negative patients. The positive rate of the term urine casts, elevated IgM and IgA in anti-alpha-actinin Abs-positive patients were higher than that in the negative patients. The OD values of serum anti-alpha-actinin Abs negatively correlated with disease activity (R(s) = -0.352, P = 0.035). Anti-alpha-actinin Abs may be a useful marker of the disease activity of SLE; in addition, it may be used as a complementary parameter to differentiate LN from SLE without nephritis.
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