الفهرس 
IntroductionOnly 14 pages are availabe for public view
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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 TGF-β was suggested as a novel biomarker. TGF-β 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 TGF-β is a major promoter of inflammation, renal injury, and fibrosis in diabetic nephropathy. Many studies showed that TGF-β expression is increased in patients with LN. Also, other studies detected high levels of TGF-β in urine samples of patients with active lupus nephritis. Urinary TGF-β is considered a potential biomarker for LN as it plays a major role in the pathogenesis of LN. TGF-β could be also a predictor for renal flares of LN. Some studies showed increased levels of TGF-β about 2-4 months before the flare and decreased after clinical remission by steroid therapy. Other studies also suggested that the level of urinary TGF-β could reflect the disease activity and differentiate patient with or without nephritis. Patients and Methods: This study was conducted on 61 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 TGF-β. 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 TGF-β increased in LN patients more than lupus non nephritis & healthy controls.Higher urinary TGF-β level can be used in prediction of LN development among SLE cases. Urinary TGF-β follow up in LN patients showed a significant decrease after treatment and this was not related to therapy. Logistic regression analysis was conducted for prediction of LN development using age, gender, SLEDAI, ANA, DNA, C3, C4, urinary protein, ACR and urinary TGF-β as covariates. Higher urinary TGF-β level was considered as risk predictor for LN development among SLE cases. Linear regression analysis was conducted for prediction of ACR improvement after treatment among LN cases using age, gender, SLEDAI, ANA, DNA, C3, C4, urinary protein, ACR and urinary TGF-β as covariates. None was considered as risk predictor for ACR improvement after treatment among LN cases. Conclusion: This study proved that urinary TGF-β increased in LN patients more than lupus non nephritis & healthy controls. Higher urinary TGF-β level can be used in prediction of LN development among SLE cases. Urinary TGF-β follow up in LN patients showed a significant decrease after treatment and this was not related to therapy. Key words: lupus nehritis, Urinary TGF-β , SLEDAI ,induction therapy.