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D'Elia JA, Bayliss G, Gleason RE, et al. Cardiovascular-renal complications and the possible role of plasminogen activator inhibitor: a review. Clin Kidney J. 2016;9(5):705-12doi: 10.1093/ckj/sfw080.
D'Elia, J. A., Bayliss, G., Gleason, R. E., & Weinrauch, L. A. (2016). Cardiovascular-renal complications and the possible role of plasminogen activator inhibitor: a review. Clinical kidney journal, 9(5), 705-12. https://doi.org/10.1093/ckj/sfw080
D'Elia, John A, et al. "Cardiovascular-renal complications and the possible role of plasminogen activator inhibitor: a review." Clinical kidney journal vol. 9,5 (2016): 705-12. doi: https://doi.org/10.1093/ckj/sfw080
D'Elia JA, Bayliss G, Gleason RE, Weinrauch LA. Cardiovascular-renal complications and the possible role of plasminogen activator inhibitor: a review. Clin Kidney J. 2016 Oct;9(5):705-12. doi: 10.1093/ckj/sfw080. Epub 2016 Aug 31. PMID: 27679717; PMCID: PMC5036907.
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Clin Kidney J. 2016 Oct;9(5):705-12. doi: 10.1093/ckj/sfw080. Epub 2016 Aug 31.

Cardiovascular-renal complications and the possible role of plasminogen activator inhibitor: a review.

Clinical kidney journal

John A D'Elia, George Bayliss, Ray E Gleason, Larry A Weinrauch

Affiliations

  1. Joslin Diabetes Center, Boston, MA, USA; Beth Israel Deaconess Medical Center, Boston, MA, USA; Harvard Medical School, Boston, MA, USA.
  2. Division ofKidney Diseases and Hypertension, Rhode Island Hospital, 593 Eddy Street, Providence, RI 02903, USA; The Miriam Hospital, Providence, RI, USA; Alpert Medical School, Brown University, Providence, RI, USA.
  3. Joslin Diabetes Center, Boston, MA, USA; Beth Israel Deaconess Medical Center, Boston, MA, USA; EP Joslin Research Laboratory, Boston, MA, USA; Brigham and Women's Hospital, Boston, MA, USA.
  4. Joslin Diabetes Center, Boston, MA, USA; Beth Israel Deaconess Medical Center, Boston, MA, USA; Harvard Medical School, Boston, MA, USA; EP Joslin Research Laboratory, Boston, MA, USA; Brigham and Women's Hospital, Boston, MA, USA.

PMID: 27679717 PMCID: PMC5036907 DOI: 10.1093/ckj/sfw080

Abstract

Since 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.

Keywords: cardiovascular; end-stage renal disease; renin–angiotensin system; thrombosis; type 2 diabetes

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