Renal dysfunction in cirrhosis: acute kidney injury and the hepatorenal syndrome

Abstract

Renal dysfunction is a common complication of liver cirrhosis and of utmost clinical and prognostic relevance. Patients with cirrhosis are more prone to developing acute kidney injury (AKI) than the non-cirrhotic population. Pre-renal AKI, the hepatorenal syndrome type of AKI (HRS-AKI, formerly known as 'type 1') and acute tubular necrosis represent the most common causes of AKI in cirrhosis. Correct differentiation is imperative, as treatment differs substantially. While pre-renal AKI usually responds well to plasma volume expansion, HRS-AKI and ATN require different specific approaches and are associated with substantial mortality. Several paradigms, such as the threshold of 2.5 mg/dL for diagnosis of HRS-AKI, have recently been abolished and novel urinary biomarkers are being investigated in order to facilitate early and correct diagnosis and treatment of HRS-AKI and other forms of AKI in patients with cirrhosis. This review summarizes the current diagnostic criteria, as well as pathophysiologic and therapeutic concepts for AKI and HRS-AKI in cirrhosis.

Keywords: acute kidney injury; hepatorenal syndrome; liver cirrhosis.

Figure 1.

Pathophysiology of acute kidney injury (AKI) and hepatorenal syndrome (HRS) in decompensated cirrhosis. Broad arrows: vasodilation theory of ascites formation. Black arrows: ‘inflammation theory’ and further aspects of AKI development. Dashed line: impact of infections (i.e. spontaneous bacterial peritonitis) on portal hypertension. SNS, sympathetic nervous system; RAAS, renin-angiotensin-aldosterone system; SIRS, systemic inflammatory response syndrome; HRS-AKI, hepatorenal syndrome type of acute kidney injury