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      Sepsis and acute kidney injury.

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          Abstract

          Sepsis is a severe and dysregulated inflammatory response to infection characterized by end-organ dysfunction distant from the primary site of infection. Development of acute kidney injury (AKI) during sepsis increases patient morbidity, predicts higher mortality, has a significant effect on multiple organ functions, is associated with an increased length of stay in the intensive care unit, and hence consumes considerable healthcare resources. When compared with AKI of nonseptic origin, septic AKI is characterized by a distinct pathophysiology and therefore requires a different approach. Despite impressive advances in several fields of medicine, the pathophysiology, diagnostic procedures, and appropriate therapeutic interventions in sepsis are still highly debatable. Numerous immunomodulatory agents showing promise in preclinical studies fail to reduce the overwhelmingly high mortality rate of sepsis and provoke AKI when compared with other critically ill patients. Major impediments to progress in understanding, early diagnosis, and application of appropriate therapeutic modalities in sepsis-induced AKI include limited histopathologic information, few animal models that closely mimic human sepsis, and a relative shortage of specific diagnostic tools. Here we discuss the most recent advances in understanding the fundamental mechanisms of sepsis-induced AKI, characteristics of relevant animal models available, and potential therapies.

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          Author and article information

          Journal
          J Am Soc Nephrol
          Journal of the American Society of Nephrology : JASN
          American Society of Nephrology (ASN)
          1533-3450
          1046-6673
          Jun 2011
          : 22
          : 6
          Affiliations
          [1 ] Division of Nephrology, THT 647, University of Alabama at Birmingham, Birmingham, AL 35294, USA.
          Article
          ASN.2010050484
          10.1681/ASN.2010050484
          21566052
          65013cc6-f6d1-4318-b1b3-a0050be90ceb
          History

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