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|Title:||The role of renin-angiotensin system in sepsis-associated acute kidney injury: mechanisms and therapeutic implications.||Austin Authors:||Garcia, Bruno;Zarbock, Alexander;Bellomo, Rinaldo ;Legrand, Matthieu||Affiliation:||Department of Anesthesia & Peri-operative Care, Division of Critical Care Medicine, University of California, San Francisco (UCSF), San Francisco, California, USA.;Department of Intensive Care, Centre Hospitalier Universitaire de Lille, Lille, France.;Experimental Laboratory of Intensive Care, Université Libre de Bruxelles, Brussels, Belgium.
Department of Anesthesiology, Intensive Care and Pain Medicine, University Hospital of Münster, Münster, Germany.
Department of Anesthesia & Peri-operative Care, Division of Critical Care Medicine, University of California, San Francisco (UCSF), San Francisco, California, USA.
Australian and New Zealand Intensive Care Research Centre, Monash University.;Department of Critical Care, Melbourne Medical School, University of Melbourne, Melbourne, Victoria, Australia.
|Issue Date:||1-Dec-2023||Date:||2023||Publication information:||Current Opinion in Critical Care 2023-12-01; 29(6)||Abstract:||This review aims to explore the relationship between the renin angiotensin system (RAS) and sepsis-associated acute kidney injury (SA-AKI), a common complication in critically ill patients associated with mortality, morbidity, and long-term cardiovascular complications. Additionally, this review aims to identify potential therapeutic approaches to intervene with the RAS and prevent the development of AKI. Recent studies have provided increasing evidence of RAS alteration during sepsis, with systemic and local RAS disturbance, which can contribute to SA-AKI. Angiotensin II was recently approved for catecholamine resistant vasodilatory shock and has been associated with improved outcomes in selected patients. SA-AKI is a common condition that can involve disturbances in the RAS, particularly the canonical angiotensin-converting enzyme (ACE) angiotensin-II (Ang II)/angiotensin II receptor 1 (AT-1R) axis. Increased renin levels, a key enzyme in the RAS, have been shown to be associated with AKI and may also guide vasopressor therapy in shock. In patients with high renin levels, angiotensin II administration may reduce renin concentration, improve intra-renal hemodynamics, and enhance signaling through the angiotensin II receptor 1. Further studies are needed to explore the role of the RAS in SA-AKI and the potential for targeted therapies.||URI:||https://ahro.austin.org.au/austinjspui/handle/1/34031||DOI:||10.1097/MCC.0000000000001092||ORCID:||Journal:||Current Opinion in Critical Care||PubMed URL:||37861190||ISSN:||1531-7072||Type:||Journal Article|
|Appears in Collections:||Journal articles|
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