Traditional cardiovascular risk factors do not entirely account for the increased risk of atherosclerosis, the major cause of death, in systemic lupus erythematosus (SLE). In this project we want to identify new pathogenic pathways of atherosclerosis in SLE patients, by assessing the association between newly identified potential risk factors and a refined measure of subclinical atherosclerosis, soft (noncalcified) coronary plaque. Similarly over 50% of SLE patients develop lupus nephritis, including 75% of African-American SLE patients. Renal biopsy is the gold standard to determine renal activity, but is expensive, invasive, and has real risk to the patient. We hypothesize that urinary markers of renal activity will have clinical utility in human lupus nephritis, as they have in renal transplant patients and murine models of SLE. In addition we want to develop and study three new approaches to assess hypercoagulability risk (endogenous thrombogenic potential, complement activation, and platelet microparticles) to determine if these markers can predict future thrombotic events or associated with antiphospholipid antibodies.
Although the survival of SLE patients has greatly improved, permanent organ damage continues to occur in the general public. This project addresses three challenges: hardening of the arteries, blood clots, and lupus kidney disease in collaboration with other rheumatologists and radiologists.
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