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Expression of endothelial protein C receptor in cortical peritubular capillaries associates with a poor clinical response in lupus nephritis - Jill P. Buyon

The contribution of the vascular endothelium to the pathogenesis of renal injury has not been emphasized in lupus nephritis (LN). Despite potential biological insights and treatment strategies to be gained by studying the endothelium in LN, neither historic WHO classification, National Institutes of Health chronicity and activity indices (CI and AI, respectively) [1], nor recent International Society of Nephrology/Renal Pathology Society (ISN/ RPS) 2003 pathological classifications of LN [2] specifically address the state of the microvasculature in their definitions. However, recent murine data based on microarray analysis suggest that endothelial activation is a feature observed in progressive glomerulosclerosis but not in non-progressive glomerulosclerosis [3].

The membrane endothelial protein C receptor (mEPCR), an integral membrane protein with both anti-inflammatory and anti-thrombotic properties, is expressed on endothelial cells and regulates the conversion of protein C to activated protein C by presenting it to the thrombin–thrombomodulin complex [4, 5]. mEPCR is shed in a pathological state to a soluble form, sEPCR, increased levels of which have been reported in two lupus cohorts [6, 7]. Patients with LN had significantly higher levels of sEPCR than those without nephritis [7].

mEPCR expression in kidney disease has been evaluated in models of sepsis and diabetes [8, 9] but never addressed in LN. Accordingly, the current study was initiated to test the hypothesis that the presentation and course of LN is influenced by the renal microvasculature, as reflected by mEPCR expression. This was approached by immunohistological analysis of mEPCR expression in kidney biopsies in patients with all classes of LN, and by correlating the results of the immunostaining with response to therapy.

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Source: Alliance for Lupus Research
Funded Research



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