2013 Volume 4 Issue 2 Pages 107-114
The incidence of acute kidney injury (AKI) has increased annually, and the prognosis of AKI is particularly poor in cases arising in intensive care units (ICU). Implementation of blood purification does not necessarily improve the outcome of AKI, and the successive and concurrent impairment of various distant major organs such as the heart, lung, brain and liver is thought to be a factor associated with poor prognosis. In the intervention of AKI, it is therefore quite important not only to consider the indication of renoprotective and renal replacement therapies, but also to constantly monitor the possible onset of major organ impairment. Inflammatory mediators play a key role in the mechanism common to the onset of distant organ impairment caused by AKI. The inflammatory mediators induced as a result of ischemic injury and various other injuries in the kidneys are not only involved in injury localized to the kidneys, but they activate systemic innate immunity as well. Consequently, in addition to activation of Toll-like receptors, reactive oxygen species, and complements, inflammatory mediators also promote the expression of chemokines specific to each organ and induce the activation of neutrophils and macrophages, ultimately leading to abnormalities in the physiological function of each distant organ. In cases of multiple distant organ disorders due to AKI, multiple inflammatory mediators, which are most notably associated with systemic inflammatory response syndrome (SIRS), are produced, and treatments targeting a single mediator may not be expected to be sufficiently effective. Therefore, with the objective of eliminating inflammatory mediators, it has been considered important to implement hemofiltration (as a non-renal indication) from an early stage before indication of blood purification in patients at risk of developing multiple organ failure due to AKI.