Endothelial function and its implications for cardiovascular and renal disease in systemic lupus erythematosus.

Vascular manifestations associated with systemic lupus erythematosus (SLE) span a broad range, including vasculopathy. An understudied pathway of this morbidity is a repair component. Recent studies have elevated the anti-injury biomarkers, adiponectin and membrane endothelial protein C receptor (EPCR), for consideration with roles to antagonize premature atherosclerosis and SLE nephritis, respectively. For example, adiponectin was found to serve as an independent predictor of carotid plaque, and its elevations were persistent over more than one visit. Unexpectedly, this biomarker was present despite clinical quiescence. In vasculopathy as a comorbidity to SLE nephritis, the persistent expression of membrane EPCR at peritubular capillaries may represent a response to the local cues of a deficit of active protein C. Under conditions of unresolved morbidity, higher levels of adiponectin and membrane EPCR may represent a physiologic attempt to limit further endothelial damage, and the observed increase in plaque and progression of SLE nephritis represent an overwhelming of this reparative process by disease-provoking stimuli.