Abstract
Renal failure develops in ∼5% all patients referred to specialized centres with acute liver failure. The renal failure may be secondary to the liver failure itself (and is termed the hepatorenal syndrome) or the renal failure may be a secondary insult that directly affects both liver and kidney alike (for example paracetamol overdose). The pathogenesis of the hepatorenal syndrome involves the development of a hyperdynamic circulation, with a lowering of renal perfusion pressure, the activation of the sympathetic nervous system, which renders the kidneys more susceptible to modest decreases in perfusion pressure, and increased synthesis of a variety of vasoactive mediators. These mediators can cause renal vasoconstriction, but more importantly they can also decrease the glomerular capillary ultrafiltration coefficient (K1), thus causing a decline of glomerular filtration rate over and above that caused by renal vasoconstriction alone. The treatment of renal failure in acute liver failure involves the optimization of renal haemodynamics and heamofiltration. Renal failure will always recover when there is recovery of liver function, and in the absence of spontaneous hepatic recovery, liver transplantation will reverse the hepatorenal syndrome.