TY - JOUR
T1 - Renohepatic crosstalk
T2 - a review of the effects of acute kidney injury on the liver
AU - Bonavia, Anthony
AU - Stiles, Nicholas
N1 - Publisher Copyright:
© The Author(s) 2021. Published by Oxford University Press on behalf of the ERA-EDTA. All rights reserved.
PY - 2022/7/1
Y1 - 2022/7/1
N2 - Several theories regarding acute kidney injury (AKI)-related mortality have been entertained, although mounting evidence supports the paradigm that impaired kidney function directly and adversely affects the function of several remote organs. The kidneys and liver are fundamental to human metabolism and detoxification, and it is therefore hardly surprising that critical illness complicated by hepatorenal dysfunction portends a poor prognosis. Several diseases can simultaneously impact the proper functioning of the liver and kidneys, although this review will address the impact of AKI on liver function. While evidence for this relationship in humans remains sparse, we present supportive studies and then discuss the most likely mechanisms by which AKI can cause liver dysfunction. These include ‘traditional’ complications of AKI (uremia, volume overload and acute metabolic acidosis, among others) as well as systemic inflammation, hepatic leukocyte infiltration, cytokine-mediated liver injury and hepatic oxidative stress. We conclude by addressing the therapeutic implications of these findings to clinical medicine.
AB - Several theories regarding acute kidney injury (AKI)-related mortality have been entertained, although mounting evidence supports the paradigm that impaired kidney function directly and adversely affects the function of several remote organs. The kidneys and liver are fundamental to human metabolism and detoxification, and it is therefore hardly surprising that critical illness complicated by hepatorenal dysfunction portends a poor prognosis. Several diseases can simultaneously impact the proper functioning of the liver and kidneys, although this review will address the impact of AKI on liver function. While evidence for this relationship in humans remains sparse, we present supportive studies and then discuss the most likely mechanisms by which AKI can cause liver dysfunction. These include ‘traditional’ complications of AKI (uremia, volume overload and acute metabolic acidosis, among others) as well as systemic inflammation, hepatic leukocyte infiltration, cytokine-mediated liver injury and hepatic oxidative stress. We conclude by addressing the therapeutic implications of these findings to clinical medicine.
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U2 - 10.1093/ndt/gfaa297
DO - 10.1093/ndt/gfaa297
M3 - Review article
C2 - 33527986
AN - SCOPUS:85133100569
SN - 0931-0509
VL - 37
SP - 1218
EP - 1228
JO - Nephrology Dialysis Transplantation
JF - Nephrology Dialysis Transplantation
IS - 7
ER -