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Progression of subclinical and clinical cardiovascular disease in a UK SLE cohort: the role of classic and SLE-related factors
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  • Published on:
    SLE and Atherosclerosis: There Are Several Mechanisms To Highlight
    • Yusuf Z ŞENER, Cardiologist Hacettepe University Faculty of Medicine
    • Other Contributors:
      • Metin OKŞUL, Cardiologist
      • Vedat Hekimsoy, Cardiologist

    Dear editor;
    We have read with great interest the article published by Haque et al. which was about association between atherosclerotic process, cardiovascular outocomes and systemic lupus erythematosus (SLE). It is reported that only SDI score, triglyceride level and cyclophosphamide exposure was predictive for future cardiovascular events and factors related with plaque progression were defined(1).
    SLE is a multisystemic disorder and lupus nephritis is one of the main manifestions of the disease. It usually presents with proteinuria and deteriorated renal glomerular functions. Renin angiotensinogen antgiotensin system (RAAS) inhibitors are used in patients with lupus nephritis to reduce proteinuria and kidney function protection(3). Angiotensin II (AT II) has unfavorable effects on endothelial functions. AT II binds AT 1 receptors and promotes vasoconstriction and production of proinlammatory cytokines and proliferation factors. It is shown by several studies that RAAS inhibitors improves endothelial functions and induces the regression of atherosclerotic process(3).
    Microalbuminuria (MAU) and proteinuria are related with worse cardiovascular outcomes. Microalbuminuria causes endothelial dysfunction and associated with accelerated atherosclerosis(4). MESA study demonstrated that coronary calcification is significantly higher in patients with microalbuminuria than counterparts without MAU. Not only presence but also amount of MAU is associated with insu...

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    Conflict of Interest:
    None declared.