Acute kidney injury: prediction, prognostication and optimisation for liver transplant

Abstract

The definition and diagnostic criteria of renal dysfunction in cirrhosis have undergone significant recent changes. Acute kidney injury (AKI) is defined by a change in serum creatinine of ≥ 26.4 µmol/L (0.3 mg/dL) in < 48 h. Its severity is defined by stages. Chronic kidney disease (CKD) is defined by a reduction in the estimated glomerular filtration rate (GFR) to < 60 mL/min for more than 3 months. Both AKI and CKD can be related to reduced renal perfusion, the so-called functional renal failure; or due to structural damage to the renal parenchyma. Hemodynamic changes and excess inflammation are the pathophysiological processes that predispose the cirrhotic patient to the development of functional AKI. Events that cause further perturbation of hemodynamics or promote further inflammation such as bacterial infection will precipitate AKI. Management starts by removing potential precipitating factors and replenish the intravascular volume. Albumin is the preferred volume expander as it has multiple properties that can significantly reduce the extent of inflammation as well as improving the intravascular volume. Non-responders to albumin infusion should receive vasoconstrictor therapy such as terlipressin, titrated to patient's blood pressure response, and is effective in approximately 50% of patients. All patients with renal and liver dysfunction should be evaluated for liver transplantation, with renal replacement therapy as a bridge. Guidelines are in place for combined liver and kidney transplants. Future studies on AKI should evaluate the effects of vasoconstrictors on renal function as defined by recent criteria, and to develop biomarkers to identify susceptible patients so to institute treatment early.

Keywords: Acute kidney injury; Albumin; Biomarkers; Chronic kidney disease; Combined liver kidney transplant; Cystatin C; Inflammation; Norepinephrine; Terlipressin; Vasoconstrictors.