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Acute kidney injury in sepsis.

  • Bellomo R School of Medicine, The University of Melbourne, Melbourne, Australia. Rinaldo.bellomo@austin.org.au.
  • Kellum JA Department of Critical Care Medicine, Center for Critical Care Nephrology, University of Pittsburgh, Pittsburgh, USA.
  • Ronco C Department of Nephrology, Dialysis and Transplantation, San Bortolo Hospital, Vicenza, Italy.
  • Wald R Division of Nephrology, St. Michael's Hospital and the University of Toronto, Toronto, Canada.
  • Martensson J Section of Anaesthesia and Intensive Care Medicine, Department of Physiology and Pharmacology, Karolinska Institutet, Stockholm, Sweden.
  • Maiden M Department of Intensive Care, Geelong University Hospital, Geelong, VIC, Australia.
  • Bagshaw SM Department of Critical Care Medicine, Faculty of Medicine and Dentistry, University of Alberta, Edmonton, Canada.
  • Glassford NJ Department of Intensive Care, Austin Hospital, Melbourne, Australia.
  • Lankadeva Y Florey Institute of Neuroscience and Mental Health, Melbourne, VIC, Australia.
  • Vaara ST Division of Intensive Care Medicine, Department of Anesthesiology, Intensive Care and Pain Medicine, University of Helsinki and Helsinki University Hospital, Helsinki, Finland.
  • Schneider A Adult Intensive Care Unit, Centre Hospitalier Universitaire Vaudois (CHUV), Lausanne, Switzerland.
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  • 2017-04-02
Published in:
  • Intensive care medicine. - 2017
Acute kidney injury
Biomarkers
Creatinine
Recovery
Renal replacement therapy
Sepsis
Acute Kidney Injury
Biomarkers
Creatinine
Critical Care
Humans
Intensive Care Units
Kidney
Kidney Function Tests
Renal Replacement Therapy
Sepsis
English 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.
Language
  • English
Open access status
green
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https://folia.unifr.ch/global/documents/259560
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