title: The histopathology of septic acute kidney injury: a systematic review.
abstract: BACKGROUND
  Sepsis is the most common trigger of acute kidney injury (AKI) in critically ill patients; understanding the structural changes associated with its occurrence is therefore important. Accordingly, we systematically reviewed the literature to assess current knowledge on the histopathology of septic AKI.
  
  
  METHODS
  A systematic review of the MEDLINE, EMBASE and CINHAL databases and bibliographies of the retrieved articles was performed for all studies describing kidney histopathology in septic AKI.
  
  
  RESULTS
  We found six studies reporting the histopathology of septic AKI for a total of only 184 patients. Among these patients, only 26 (22%) had features suggestive of acute tubular necrosis (ATN). We found four primate studies. In these, seven out of 19 (37%) cases showed features of ATN. We also found 13 rodent studies of septic AKI. In total, 23% showed evidence of ATN. In two additional studies performed in a dog model and a sheep model there was no evidence of ATN on histopathologic examination. Overall, when ATN was absent, studies reported a wide variety of kidney morphologic changes in septic AKI - ranging from normal (in most cases) to marked cortical tubular necrosis.
  
  
  CONCLUSIONS
  There are no consistent renal histopathological changes in human or experimental septic AKI. The majority of studies reported normal histology or only mild, nonspecific changes. ATN was relatively uncommon.
authors.affiliation: Department of Intensive Care, Austin Hospital, Studley Rd, Heidelberg, Melbourne, Victoria 3084, Australia. christoph.langenberg@gmail.com
authors.forename: Christoph
authors.initials: C
authors.lastname: Langenberg
authors.forename: Sean M
authors.initials: SM
authors.lastname: Bagshaw
authors.forename: Clive N
authors.initials: CN
authors.lastname: May
authors.forename: Rinaldo
authors.initials: R
authors.lastname: Bellomo
mesh_terms: D058186:Acute Kidney Injury / Q000209:etiology / Q000473:pathology*; D000818:Animals; D016638:Critical Illness; D006801:Humans; D018805:Sepsis / Q000150:complications / Q000473:pathology*