Background: Systemic lupus erythematosus is a systemic autoimmune disease with multiorgan involvement. It is commonly complicated by autoimmune glomerulonephritis in up to 70% of cases.
Objectives: The objectives of this study was to evaluate the clinical significance of soluble thrombomodulin (sTM) and serum plasminogen activator inhibitor-1 (sPA1) in Juvenile SLE patients and to explore their possible role in lupus nephritis being both related to endothelial cell dysfunction.
Methods: We measured levels of sTM and sPA1-1 in 30 SLE patients and 30 healthy age and sex matched subjects as a control group. Eighteen cases with lupus nephritis, confirmed by renal biopsy were compared with 12lupus patients without nephritis and control. Among the lupus nephritis cases, sex and class I or II nephritis as representative of mild form of lupus nephritis, and twelve with class III, IV or V as representative of severe form of lupus nephritis.
Results: We found that sTM and sPA1-1 were significantly higher in the whole SLE group compared to the control with p = 0.000. Cases with lupus nephritis showed significantly higher levels of both sTM and sPA1-1 compared to control with p ˂ 0.049 and 0.01 respectively. When we considered the class of lupus nephritis, sTM showed a statistically significant difference between cases with class III, IV & V nephritis versus control and nephritis –ve cases with p = 0.000 and ˂ 0.003 respectively. Regarding sPA1-1, statistical analysis revealed significantly higher levels in cases with class III, IV & V compared to control, nephritis –ve, and class I and II patients with p = 0.000. Also, sTM was significantly higher in cases with disease                activity, proteinuria, endo capillary, hypercellularity, interstitial mononuclear cell infiltration, tubular atrophy, and interstitial fibrosis compared to without, with p ˂ 0.004, 0.04, 0.03, 0.04, 0.000 and 0.000 respectively. A statistically difference of sPA1-1 was found in lupus patients with and without, proteinuria, urinary casts, endo capillary hypercellularity, interstitial mononuclear cell infiltration, tubular atrophy, glomerulosclerosis. And interstitial fibrosis with p ˂ 0.027, 0.048, 0.000, 0.000, 0.001, 0.014 and 0.000 respectively.
Conclusions: In conclusion, our results suggest that dysregulation of the coagulation and fibrinolytic system may be an important mediator of glomerular injury in lupus nephritis and it seems that the more severe and active the kidney lesion, the higher the levels of sTM and sPA1-1, thus, indicating more advanced degree of vasculitis.