الفهرس 
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Abstract
Background: • SLE is a chronic inflammatory disease that could affect the kidney and cause LN in about 50% of the patients. The prevalence of SLE and the chance to develop LN vary between different regions, races, and ethnicities. Different risk factors were suggested for SLE developing e.g. race, socioeconomic state, genetic factors, and smoking. LN is a major factor of morbidity and mortality in SLE patients as ESRD will develop in 10% of patient with LN. Time to develop LN in SLE patients is not known definitely. LN may be presented at the time of SLE diagnosis or during the disease course. Many trials were done for early diagnosis and prediction the occurrence of LN. Many biomarkers were suggested but no one could replace renal biopsy up till now. The ideal biomarker should be specific, cost effective, easy to perform and superior to conventional parameters. Urinary MCP-1 was suggested as a novel biomarker. MCP-1 is a pro inflammatory chemokine that has a role in acute and chronic phases of inflammation by recruitment of monocyte and T-lymphocyte. It was proved that MCP-1 is a major promoter of inflammation, renal injury, and fibrosis in diabetic nephropathy. Many studies showed that MCP-1 expression is increased in patients with LN. Also, other studies detected high levels of MCP-1 in urine samples of patients with active lupus nephritis. Urinary MCP-1 is considered a potential biomarker for LN as it plays a major role in the pathogenesis of LN. MCP-1 could be also a predictor for renal flares of LN. Some studies showed increased levels of MCP-1 about 2-4 months before the flare and decreased after clinical remission by steroid therapy. Other studies also suggested that the level of urinary MCP-1 could reflect the disease activity and differentiate patient with or without nephritis. Patients and Methods: This study was conducted on 60 patients and divided into three equal groups: control group, lupus non nephritis group and lupus nephritis group. All patients were subjected to Detailed history taking and systemic physical examination, Assessment of disease activity by SLE disease activity index (SLEDAI)and Laboratory investigations including as Serum creatinine, Urine analysis and 24h urinary protein,CBC, ESR and CRP,ANA, anti-dsDNA, serum C3, and C4 and Urinary MCP-1 to urinary creatinine excretion. Patients with LN underwent kidney biopsy and induction therapy by either MMF or Endoxan and were followed up after six months by SLEADI and the same laboratory investigation done at enrollment. Results: Our study also showed that that MCP1/creatinine ratio can discriminate patients with lupus nephritis from those without nephritis and from healthy control subjects, but it cannot discriminate lupus without nephritis from healthy control subjects. Binary logistic regression analysis which was run to ascertain the effects of MCP-creatinine ratio at enrollment, SLEDAI at enrollment, ANA folds at enrollment and Anti-dsDNA folds at enrollment on the likelihood that participants (SLE cases) will exhibit nephropathy.A binary logistic regression analysis was run to ascertain the effects of Mcp-creatinine ratio, SLEDAI, ANA folds and Anti-dsDNA folds after 6 months and the type of induction regimen on the likelihood that lupus nephritis cases will achieve renal remission either partial or complete. The univariate analysis showed that none of these factors was a significant predictor of renal response after 6 months.Finally, no statistically significant correlation between Mcp-1creatinine ratio, SLEDAI, and histopathological activity and chronicity index was observed. Conclusion: This study proved that urinary MCP/Creatinine ratio increased in LN patients more than either lupus non nephritis or healthy controls. Urinary MCP-1 follow up in LN patients showed a significant decrease after treatment and this was not related to either line of therapy (MMF vs Cyclophosphamide).