Abstract
Acute liver failure is a rare and often devastating condition consequent on massive liver cell necrosis that frequently affects young, previously healthy individuals resulting in altered cognitive function, coagulopathy and peripheral vasodilation. These patients frequently develop concurrent acute kidney injury (AKI). This abrupt and sustained decline in renal function, through a number of pathogenic mechanisms such as renal hypoperfusion, direct drug-induced nephrotoxicity or sepsis/systemic inflammatory response contributes to increased morbidity and is strongly associated with a worse prognosis. Improved understanding of the pathophysiology AKI in the context of acute liver failure may be beneficial in a number of areas; the development of new and sensitive biomarkers of renal dysfunction, refining prognosis and organ allocation, and ultimately leading to the development of novel treatment strategies, these issues are discussed in more detail in this expert review.
Financial & competing interests disclosure
The authors have no relevant affiliations or financial involvement with any organization or entity with a financial interest in or financial conflict with the subject matter or materials discussed in the manuscript. This includes employment, consultancies, honoraria, stock ownership or options, expert testimony, grants or patents received or pending or royalties.
No writing assistance was utilized in the production of this manuscript.
• Acute kidney injury (AKI) is a common complication of acute liver failure (ALF).
• AKI is associated with adverse clinical outcomes in this clinical situation. AKI is associated with longer hospital stays and increased mortality, but does not appear to result in increased risk of chronic renal failure during long-term follow-up.
• Acetaminophen-induced ALF is the most common etiology of ALF associated with AKI and the kidneys should always be considered ‘at risk’ in such patients.
• Studies show that adequate fluid replacement is essential and continuous renal replacement therapy is preferable to intermittent dialysis due to the risk of hypotensive episodes and risk of aggravating intracranial hypertension.
• Biomarkers for renal injury remain an area of study and might aid early diagnosis and clinical decision-making regarding the use of renal replacement therapy and liver transplant allocation.
• Further targets for future therapies include renal ammonia excretion, tubular cell death and renal inflammation.
• Hope also remains that a successful external hepatic replacement therapy may be developed in the future for clinical practice allowing greater numbers of critically ill patients to survive until a liver transplant becomes available or potentially replace transplantation completely.
Notes
NAG: N-acetyl-β-d-glucosaminidase; NGAL: Neutrophil gelatinase-ssociated lipocalin; RRT: Renal replacement therapy.