Abstract
IntroductionSepsis 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.MethodsA 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.ResultsWe 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.ConclusionThere 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.
Highlights
Sepsis is the most common trigger of acute kidney injury (AKI) in critically ill patients; understanding the structural changes associated with its occurrence is important
We found six studies reporting the histopathology of septic AKI for a total of only 184 patients
Overall, when acute tubular necrosis (ATN) was absent, studies reported a wide variety of kidney morphologic changes in septic AKI – ranging from normal to marked cortical tubular necrosis
Summary
Sepsis is the most common trigger of acute kidney injury (AKI) in critically ill patients; understanding the structural changes associated with its occurrence is important. Acute kidney injury (AKI) is a common clinical problem in critically ill patients [1,2]. Sepsis is the most important contributing factor for the development of AKI in the critically ill population [3]. Ischemia followed by acute tubular necrosis (ATN), have been repeatedly proposed as central to septic AKI development [4,5]. A possible strategy aimed at gaining better insight into the pathogenesis of septic AKI could be based on developing a clearer appreciation of the histopathological changes that occur in this condition. No comprehensive review of the histopathological features of septic AKI has yet been performed
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