Sepsis-Induced Acute Kidney Injury Johan Mårtensson, MD, PhD, DESA a,b , Rinaldo Bellomo, MD, FRACP, FCICM a,c, * INTRODUCTION Severe sepsis is the trigger for the development of approximately 50% of cases of acute kidney injury (AKI) among critically ill patients. 1 Even in patients with less severe infections, the incidence of AKI is as high as 16% to 25%. 2 Sepsis-induced AKI is associated with mortality rates of up to 50% to 60%, depending on severity. 3 Septic AKI is characterized by a rapid and often profound decline in the kidneys’ ability to fil- ter blood and eliminate nitrogen waste products, usually evolving over hours to days after the onset of sepsis. 4 Limited understanding of pathophysiologic mechanisms has precluded the development of effective therapies for sepsis-induced AKI. However, Conflicts of Interest: None declared. a Department of Intensive Care, Austin Hospital, 145 Studley Road, Heidelberg, Victoria 3084, Australia; b Department of Physiology and Pharmacology, Section of Anaesthesia and Intensive Care Medicine, Karolinska Institutet, 171 77 Stockholm, Sweden; c Department of Epidemi- ology and Preventive Medicine, Australian and New Zealand Intensive Care Research Centre, School of Preventive Medicine and Public Health, Monash University, 99 Commercial Road, Mel- bourne, Victoria 3004, Australia * Corresponding author. Department of Epidemiology and Preventive Medicine, Australian and New Zealand Intensive Care Research Centre, Monash University, Melbourne, Australia. E-mail addresses: rinaldo.bellomo@monash.edu; rinaldo.bellomo@austin.org.au KEYWORDS  Sepsis  Acute kidney injury  Inflammation  Renal replacement therapy KEY POINTS  Acute kidney injury (AKI) is a common and potentially fatal complication of sepsis.  Sepsis-induced immune cells seems to release reactive oxygen and nitrogen species, which can damage tubular cells directly.  Nephrons seem to adapt to sepsis-induced renal stress by conserving energy, removing dysfunctional cells, decreasing the glomerular filtration rate, and possibly recruiting shunt pathways, which attenuate their contact with toxin-rich blood.  It is likely that progression of septic AKI can, in part, be prevented by avoiding hypoten- sion, fluid overload, and venous congestion.  Future therapeutic options for septic AKI may include antiinflammatory drugs targeting molecular mechanisms involved in the pathogenesis of septic AKI, and/or blood purification techniques. Crit Care Clin - (2015) -–- http://dx.doi.org/10.1016/j.ccc.2015.06.003 criticalcare.theclinics.com 0749-0704/15/$ – see front matter Ó 2015 Elsevier Inc. All rights reserved.