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Indexed/Abstracted in: CAB, EMBASE, PubMed/MEDLINE, Scopus, Emerging Sources Citation Index
Online ISSN 1827-1642
Division of Gastroenterology, Department of Medicine, Toronto General Hospital, University Health Network, Toronto, Ontario, Canada
Renal dysfunction in cirrhosis is mostly related to the development of acute kidney injury (AKI), precipitated by either an acute disturbance of hemodynamics, or acute structural damage to the kidneys. The incidence of chronic renal failure is rising, due to increasing prevalence of conditions such as diabetes, viral hepatitis, which can be associated with renal damage. AKI is defined as a rise in serum creatinine of 0.3 mg/dL in <48 hours or by 50% from baseline within the past 3 months without setting a threshold for the final serum creatinine. Stages 1, 2, and 3 of AKI are defined as 150%, 200% and 300% of baseline serum creatinine respectively, which allows for assessment of AKI progression. Chronic kidney disease (CKD) is defined as an estimated glomerular filtration rate of <60 mL/min for >3 months. Treatment of AKI consists of removal of precipitating factors and replenishment of the intravascular volume using colloids such as albumin. Frequently, AKI can be reversed using these measures alone. Non-responders to removal of precipitating factors and volume challenge can receive vasoconstrictors such as terlipressin or norepinephrine together with albumin. Midodrine is inferior in efficacy as a vasoconstrictor when compared to terlipressin. Liver transplantation is the definitive treatment for type 1 hepatorenal syndrome with liver failure. Delay in receiving a liver transplant can result in non-recovery of renal function post transplant. Treatment of CKD in cirrhosis is unsatisfactory, mostly aimed at optimizing management of comorbid conditions, or treating the underlying refractory ascites in patients with type 2 hepatorenal syndrome.