Please use this identifier to cite or link to this item: http://ahro.austin.org.au/austinjspui/handle/1/17359
Title: Acute kidney injury in sepsis.
Authors: Bellomo, Rinaldo;Kellum, John A;Ronco, Claudio;Wald, Ron;Martensson, Johan;Maiden, Matthew;Bagshaw, Sean M;Glassford, Neil J;Lankadeva, Yugeesh;Vaara, Suvi T;Schneider, Antoine
Affiliation: School of Medicine, The University of Melbourne, Melbourne, Australia
Department of Intensive Care, Austin Health, Heidelberg, Victoria, Australia
Department of Critical Care Medicine, Center for Critical Care Nephrology, University of Pittsburgh, Pittsburgh, USA
Department of Nephrology, Dialysis and Transplantation, San Bortolo Hospital, Vicenza, Italy
International Renal Research Institute of Vicenza (IRRIV) San Bortolo Hospital, Vicenza, Italy
Division of Nephrology, St. Michael's Hospital and the University of Toronto, Toronto, Canada
Li Ka Shing Knowledge Institute of St. Michael's Hospital, Toronto, Canada
Section of Anaesthesia and Intensive Care Medicine, Department of Physiology and Pharmacology, Karolinska Institutet, Stockholm, Sweden
Department of Intensive Care, Geelong University Hospital, Geelong, VIC, Australia
Department of Intensive Care, Royal Adelaide Hospital, Adelaide, SA, Australia
Department of Critical Care Medicine, Faculty of Medicine and Dentistry, University of Alberta, Edmonton, Canada
Department of Epidemiology and Preventive Medicine, Australian and New Zealand Intensive Care Research Centre, Monash University, Melbourne, Australia
Florey Institute of Neuroscience and Mental Health, Melbourne, VIC, Australia
Division of Intensive Care Medicine, Department of Anesthesiology, Intensive Care and Pain Medicine, University of Helsinki and Helsinki University Hospital, Helsinki, Finland
Adult Intensive Care Unit, Centre Hospitalier Universitaire Vaudois (CHUV), Lausanne, Switzerland
Issue Date: Jun-2017
EDate: 2017-03-31
Citation: Intensive care medicine 2017; 43(6): 816-828
Abstract: Acute kidney injury (AKI) and sepsis carry consensus definitions. The simultaneous presence of both identifies septic AKI. Septic AKI is the most common AKI syndrome in ICU and accounts for approximately half of all such AKI. Its pathophysiology remains poorly understood, but animal models and lack of histological changes suggest that, at least initially, septic AKI may be a functional phenomenon with combined microvascular shunting and tubular cell stress. The diagnosis remains based on clinical assessment and measurement of urinary output and serum creatinine. However, multiple biomarkers and especially cell cycle arrest biomarkers are gaining acceptance. Prevention of septic AKI remains based on the treatment of sepsis and on early resuscitation. Such resuscitation relies on the judicious use of both fluids and vasoactive drugs. In particular, there is strong evidence that starch-containing fluids are nephrotoxic and decrease renal function and suggestive evidence that chloride-rich fluid may also adversely affect renal function. Vasoactive drugs have variable effects on renal function in septic AKI. At this time, norepinephrine is the dominant agent, but vasopressin may also have a role. Despite supportive therapies, renal function may be temporarily or completely lost. In such patients, renal replacement therapy (RRT) becomes necessary. The optimal intensity of this therapy has been established, while the timing of when to commence RRT is now a focus of investigation. If sepsis resolves, the majority of patients recover renal function. Yet, even a single episode of septic AKI is associated with increased subsequent risk of chronic kidney disease.
URI: http://ahro.austin.org.au/austinjspui/handle/1/17359
DOI: 10.1007/s00134-017-4755-7
ORCID: 0000-0002-1650-8939
0000-0001-8739-7896
PubMed URL: 28364303
Type: Journal Article
Review
Subjects: Acute kidney injury
Biomarkers
Creatinine
Recovery
Renal replacement therapy
Sepsis
Appears in Collections:Journal articles

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