Literature review of the mechanisms of acute kidney injury secondary to acute liver injury

Abstract

People exposed to liver ischaemia reperfusion (IR) injury often develop acute kidney injury and the combination is associated with significant morbidity and mortality. Molecular mediators released by the liver in response to IR injury are the likely cause of acute kidney injury (AKI) in this setting, but the mediators have not yet been identified. Identifying the mechanism of injury will allow the identification of therapeutic targets which may modulate both liver IR injury and AKI following liver IR injury.

Keywords: Acute kidney injury; Ischaemia-reperfusion injury; Liver; Liver failure; Liver transplantation.

Figure 1

Schematic representation of current evidence to support the mechanistic link between liver IR injury and resultant kidney injury. The evidence for the possible mediators of injury detailed in this diagram will be discussed in more detail in the text of this review. A summary of the major studies discussed in this review can also be found in Supplementary Table 1.

Figure 2

Diagrammatic representation of the current understanding of histological changes within the kidney that accompany acute kidney injury following liver ischaemia reperfusion injury. These data are obtained from animal studies. To date no objective grading system for histological severity of injury has been developed which means that only limited comparison of injury severity between studies is possible. Development of an objective scoring system across the first 48 h of renal injury would be of great benefit in this field of research.