The Association between Serum Lipoxin A4 Level and Lupus Nephritis

Abstract
Background: Systemic Lupus Erythematosus (SLE) is an autoimmune connective tissue disorder with a wide range of clinical features, which predominantly affects females. Glomer-ulonephritis (GN) is a major determinant of the course and prognosis of SLE and is clinically evident in 40-83% of patients. Lupus Nephritis (LN) affects from one-third to one-half of lupus patients and accounts for significant morbidity and mortality. Lipoxins are produced locally at sites of in-flammation by transcellular routes. Lipoxin biosynthesis has been described in many human and experimental diseases associated with cell contact, including glomerulonephritis, asthma, and rheumatoid arthritis. Yet, there is no gold standard for assessment of lupus nephritis up till now.
Aim of Study: The aim of this study is to assess the level of serum lipoxin A4 as a diagnostic biomarker in cases of SLE complicated with lupus nephritis and to evaluate its relation to pathogenesis of lupus nephritis and renal disease activity.
Patients and Methods: This study was conducted on fifty Egyptian patients with Lupus Nephritis (LN) and 10 healthy subjects as a control. Disease activity was assessed using Systemic Lupus Erythematosus Disease Activity Index (SLEDAI) and renal SLEDAI. Complete blood picture (CBC), ESR, Anti deoxyribonucleic acid (Anti-dsDNA) antibodies, Antinuclear Antibodies (ANA), quantitative determination of serum complements levels (C3, C4), complete urine analysis, 24 hours urinary proteins, serum creatinine, blood urea and Serum Lipoxin A4 (LXA4) level by (ELISA) were done for all samples of the study groups. Renal biopsy, microscopic examination and pathological classification was performed for all patients.
Results: SLE patients with lupus nephritis showed a lower median level of serum LXA4 compared with the control group (7.7 Vs. 25.8ng/ml), with highly significant statistical differ-ence (p<0.001). Total SLEDAI and the renal SLEDAI, also were correlated with lipoxin A4 level and showed no significant statistical correlation. No correlation was found between serum lipoxin A4 and, age, sex, disease duration, anti-dsDNA, C3 and C4, ESR, 24 urinary proteins, ANA and CBC param-eters. The levels of serum lipoxin A4 did not show significant statistical difference among all SLE patients and the drug history.
Conclusion: Serum LXA4 deficiency could be used as a noninvasive diagnostic biomarker for renal involvement in SLE patients.