Figure 1.

The vasodilatation hypothesis of hepatorenal syndrome. (Adapted from Wong et al.¹³). In cirrhosis, portal hypertension leads to splanchnic and systemic vasodilatation, which results in a decrease in effective arterial volume. This in turn leads to the activation of vasoconstrictor systems leading to a reduction in renal blood flow. An impairment of cardiac function (cirrhotic cardiomyopathy) and abnormal renal blood flow autoregulation further contributes to renal hypoperfusion, resulting in HRS.