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      Acute kidney injury in major abdominal surgery: incidence, risk factors, pathogenesis and outcomes

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          Abstract

          Acute kidney injury (AKI) is a common complication in patients undergoing major abdominal surgery. Various recent studies using modern standardized classifications for AKI reported a variable incidence of AKI after major abdominal surgery ranging from 3 to 35%. Several patient-related, procedure-related factors and postoperative complications were identified as risk factors for AKI in this setting. AKI following major abdominal surgery has been shown to be associated with poor short- and long-term outcomes. Herein, we provide a contemporary and critical review of AKI after major abdominal surgery focusing on its incidence, risk factors, pathogeny and outcomes.

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          Acute kidney injury, mortality, length of stay, and costs in hospitalized patients.

          The marginal effects of acute kidney injury on in-hospital mortality, length of stay (LOS), and costs have not been well described. A consecutive sample of 19,982 adults who were admitted to an urban academic medical center, including 9210 who had two or more serum creatinine (SCr) determinations, was evaluated. The presence and degree of acute kidney injury were assessed using absolute and relative increases from baseline to peak SCr concentration during hospitalization. Large increases in SCr concentration were relatively rare (e.g., >or=2.0 mg/dl in 105 [1%] patients), whereas more modest increases in SCr were common (e.g., >or=0.5 mg/dl in 1237 [13%] patients). Modest changes in SCr were significantly associated with mortality, LOS, and costs, even after adjustment for age, gender, admission International Classification of Diseases, Ninth Revision, Clinical Modification diagnosis, severity of illness (diagnosis-related group weight), and chronic kidney disease. For example, an increase in SCr >or=0.5 mg/dl was associated with a 6.5-fold (95% confidence interval 5.0 to 8.5) increase in the odds of death, a 3.5-d increase in LOS, and nearly 7500 dollars in excess hospital costs. Acute kidney injury is associated with significantly increased mortality, LOS, and costs across a broad spectrum of conditions. Moreover, outcomes are related directly to the severity of acute kidney injury, whether characterized by nominal or percentage changes in serum creatinine.
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            Mechanisms of maladaptive repair after AKI leading to accelerated kidney ageing and CKD.

            Acute kidney injury is an increasingly common complication of hospital admission and is associated with high levels of morbidity and mortality. A hypotensive, septic, or toxic insult can initiate a cascade of events, resulting in impaired microcirculation, activation of inflammatory pathways and tubular cell injury or death. These processes ultimately result in acutely impaired kidney function and initiation of a repair response. This Review explores the various mechanisms responsible for the initiation and propagation of acute kidney injury, the prototypic mechanisms by which a substantially damaged kidney can regenerate its normal architecture, and how the adaptive processes of repair can become maladaptive. These mechanisms, which include G2/M cell-cycle arrest, cell senescence, profibrogenic cytokine production, and activation of pericytes and interstitial myofibroblasts, contribute to the development of progressive fibrotic kidney disease. The end result is a state that mimics accelerated kidney ageing. These mechanisms present important opportunities for the design of targeted therapeutic strategies to promote adaptive renal recovery and minimize progressive fibrosis and chronic kidney disease after acute insults.
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              Association of intraoperative hypotension with acute kidney injury after elective noncardiac surgery.

              Intraoperative hypotension (IOH) may be associated with postoperative acute kidney injury (AKI), but the duration of hypotension for triggering harm is unclear. The authors investigated the association between varying periods of IOH with mean arterial pressure (MAP) less than 55, less than 60, and less than 65 mmHg with AKI.
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                Author and article information

                Contributors
                joana.estrelagameiro@gmail.com
                jose.nuno.agapito@gmail.com
                martaraq_neves@hotmail.com
                sofiacjorge@sapo.pt
                jalopes93@hotmail.com
                Journal
                Ann Intensive Care
                Ann Intensive Care
                Annals of Intensive Care
                Springer International Publishing (Cham )
                2110-5820
                9 February 2018
                9 February 2018
                2018
                : 8
                : 22
                Affiliations
                ISNI 0000 0004 0474 1607, GRID grid.418341.b, Division of Nephrology and Renal Transplantation, Department of Medicine, , Centro Hospitalar Lisboa Norte, EPE, ; Av. Prof. Egas Moniz, 1649-035 Lisbon, Portugal
                Article
                369
                10.1186/s13613-018-0369-7
                5807256
                29427134
                5cdca0c7-06e5-414e-b7a0-9b53a17db566
                © The Author(s) 2018

                Open AccessThis article is distributed under the terms of the Creative Commons Attribution 4.0 International License ( http://creativecommons.org/licenses/by/4.0/), which permits unrestricted use, distribution, and reproduction in any medium, provided you give appropriate credit to the original author(s) and the source, provide a link to the Creative Commons license, and indicate if changes were made.

                History
                : 31 October 2017
                : 5 February 2018
                Categories
                Review
                Custom metadata
                © The Author(s) 2018

                Emergency medicine & Trauma
                acute kidney injury,postoperative,incidence,prognosis,risk factors,pathogenesis

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