Sepsis-Induced Acute Kidney Injury

J. A. Smith, R. G. Schnellmann

Research output: Chapter in Book/Report/Conference proceedingChapter

Abstract

Sepsis is broadly defined as the systemic inflammatory response to known or suspected infection. It remains a common cause of both morbidity and mortality in the critical care setting. Injury to multiple organ systems including the kidneys, liver, lungs, and brain is an important consequence of the overwhelming inflammatory response in sepsis. Current estimates indicate that acute kidney injury (AKI) occurs in approximately 60% of septic patients and significantly increases the risk of sepsis-associated mortality. Despite extensive laboratory and clinical study, therapy for sepsis and septic AKI remains limited to supportive measures. The purpose of this article is to review current understanding of the pathophysiology of AKI and sepsis and highlight areas where further work is needed. Important concepts, definitions, epidemiology, and experimental models of sepsis-induced AKI are introduced. The molecular mechanisms underlying sepsis-induced AKI are then extensively reviewed. Finally, we focus on the emerging role of mitochondrial dysfunction in septic AKI and discuss mitochondrial dynamics as a novel therapeutic target in this disease.

Original languageEnglish (US)
Title of host publicationRenal Toxicology
PublisherElsevier Inc.
Pages128-146
Number of pages19
Volume14-15
ISBN (Electronic)9780081006122
ISBN (Print)9780081006016
DOIs
StatePublished - 2018

Keywords

  • Acute kidney injury
  • Biomarkers
  • Cytokines
  • Epidemiology
  • Experimental models
  • Glycolysis
  • Hemodynamics
  • Inflammation
  • Microvascular dysfunction
  • Mitochondrial biogenesis
  • Mitochondrial dynamics
  • Pharmacotherapy
  • Renal proximal tubule
  • Sepsis
  • Toll-like receptors

ASJC Scopus subject areas

  • Medicine(all)

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