In cirrhosis and fulminant hepatic failure acute renal failure may occur both without ("functional renal failure") and with tubular necrosis, the two probably being the ends of a spectrum. The underlying pathophysiological change is an intense renal and intra-renal vasoconstriction. Evidence is presented that this is due to systemic endotoxaemia resulting from failure of the liver to filter endotoxins absorbed from the gastrointestinal tract. Acute renal failure complicating obstructive jaundic has also been related to endotoxaemia, but in contrast to cirrhosis and fulminant hepatic failure this is usually due to an associated gram-negative infection and the renal failure almost invariably has the features of acute tubular necrosis. Endotoxins have two major effects on the kidney: (i) renal vasoconstriction, and (ii) glomerular and peritubular fibrin deposition. The nature of the renal failure depends on the balance between these variables which may be profoundly altered by the underlying liver disease.