Hugo Tanno

Over a hundred years ago Austin Flint described the association between chronic liver disease and kidney failure. Since then, much progress has been made in the pathophysiological knowledge of what is universally known as hepatorenal syndrome.

This syndrome is recognized as an entity in cirrhotic patients (more often alcoholic) who develop, in advanced stages of the disease, a progressive renal failure that is the cause of death in approximately 10% of them. It is interesting to highlight the absence of important organic lesions in the kidney of these patients, which led some authors to call this progressive renal failure functional renal failure.

This syndrome can be identified by its clinical and laboratory characteristics.

The symptoms are those that usually accompany the advanced stages of cirrhosis, to which are added some very significant ones such as marked asthenia, anorexia, moderate ascites, little jaundice, neurological manifestations of metabolic encephalopathy (tremor, asterixis) due to increased plasma ammonia and other toxic by-products, etc. This condition is more frequent in patients treated with diuretics, and poor medical management of an ascitic-edematous syndrome may be the trigger.

Renal failure is manifested by marked oliguria (sometimes fixed diuresis less than 800 ml / day) and a progressive elevation of plasma levels of urea, creatinine and potassium, which highlights the difficulty that the kidney has to correctly comply with its purifying function.

This florid clinical picture is not accompanied by an important organic kidney disease and few are the anatomical alterations so far described in vast series of neocropsies. For this reason, the kidneys of dead cirrhotic patients with a hepatorenal syndrome have been shown to be viable for transplantation in anephritic subjects.

The pathophysiology of functional renal failure is complex and its description exceeds the limits of this synthesis; However, the role that renal hemodynamic disorders play in the genesis of the syndrome in cirrhotic patients seems evident. A large shunt of blood from the cortex to the renal medulla has been seen, which deprives the periphery of the kidney of the rich cortical flow that characterizes the organ of a normal subject.

This phenomenon, which is usually evolutionary, progressively leads to kidney failure and death to cirrhotic disease.

The syndrome is rarely reversible. Mortality exceeds 98%, and at the moment there is no effective therapy to encourage favorable expectations.