D'Elia, JohnBayliss, GeorgeGleason, RayWeinrauch, Larry2016-11-182016D'Elia, John A., George Bayliss, Ray E. Gleason, and Larry A. Weinrauch. 2016. “Cardiovascular-renal complications and the possible role of plasminogen activator inhibitor: a review.” Clinical Kidney Journal 9 (5): 705-712. doi:10.1093/ckj/sfw080. http://dx.doi.org/10.1093/ckj/sfw080.2048-8505http://nrs.harvard.edu/urn-3:HUL.InstRepos:29407618Since angiotensin increases the expression of plasminogen activator inhibitor (PAI), mechanisms associated with an actively functioning renin–angiotensin–aldosterone system can be expected to be associated with increased PAI-1 expression. These mechanisms are present not only in common conditions resulting in glomerulosclerosis associated with aging, diabetes or genetic mutations, but also in autoimmune disease (like scleroderma and lupus), radiation injury, cyclosporine toxicity, allograft nephropathy and ureteral obstruction. While the renin–angiotensin–aldosterone system and growth factors, such as transforming growth factor-beta (TGF-β), are almost always part of the process, there are rare experimental observations of PAI-1 expression without their interaction. Here we review the literature on PAI-1 and its role in vascular, fibrotic and oxidative injury as well as work suggesting potential areas of intervention in the pathogenesis of multiple disorders.en-UScardiovascularend-stage renal diseaserenin–angiotensin systemthrombosistype 2 diabetesJournal Article2016-11-1810.1093/ckj/sfw080