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Arch Hellen Med, 33(1), January-February 2016, 22-38


Acute kidney injury in patients with cirrhosis of the liver

S. Papadaki, S.P. Dourakis
Second Department of Internal Medicine, National and Kapodistrian University of Athens, Medical School,"Hippokration" General Hospital, Athens, Greece

In recent years important steps have been made in understanding the pathogenesis of acute renal failure in liver cirrhosis. In particular, the implications of renal dysfunction on the prognosis of the underlying disease have been studied. New terms have been introduced in an attempt to identify more easily even the smallest changes in renal function. Acute renal failure was recently renamed acute kidney injury (ΑΚΙ) and was defined as a creatinine increase of >1.5 mg/dL or a decrease in creatinine clearance of <40 mL/min. The most frequent causes of ΑΚΙ in patients with cirrhosis include prerenal azotemia, acute tubular necrosis and hepatorenal syndrome. Despite efforts made in recent years the differential diagnosis of ΑΚΙ remains difficult, compromising the implementation of appropriate timely treatment. Prerenal azotemia is treated with volume restoration and releasing factor suspension, and acute tubular necrosis is treated symptomatically and if necessary by renal replacement therapy. The treatment approach to hepatorenal syndrome is the co-administration of vasopressors midodrine (combined with octreotide) and vasoconstrictors such as terlipressin, vasopressin or norepinephrine with albumin to improve the flow of arterial blood. Dialysis is indicated for patients with clinically significant excess fluid volume and severe electrolyte imbalance. The placement of a transjugular intrahepatic portosystemic shunt can help in selected cases. The ultimate treatment is liver transplantation. In recent years in an attempt at early diagnosis of AKI in both the general population and specific cases such as patients with cirrhosis new biomarkers have been introduced. These include lipokalin associated with neutrophil gelatinase (ΝGAL), cystatin C (CysC), kidney injury molecule 1 (KIM-1), interleukin 18 (IL-18) and the hepatic binding protein type of fatty acid (L-FABP3). Studies reported to date show encouraging results as to the usefulness of these indicators in the diagnosis, differential diagnosis, therapeutic approach to and treatment of ΑΚΙ.

Key words: Acute renal injury, Binding protein liver type fatty acids, Complications of liver cirrhosis, Cystatin C, Hepatorenal syndrome, Interleukin-18, Kidney injury molecule 1, Neutrophil gelatinase.

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