Hepatorenal syndrome (HRS) is defined as a reversible functional kidney defect that occurs in people with advanced liver disease or severe reduction of hepatic function. The drastic change in the levels of renal vasoconstrictors, splanchnic vasodilators, and the vitality of the general and systemic circulation are the pathophysiological indications of this syndrome.
The condition may endanger life if the treatment is incomplete or inappropriate. Currently, much research has been done on HRS and new treatments have been found that offer an improved prognosis. Early diagnosis of this disease can save the life of the patient. Liver transplantation and proper therapy for renal failure are the two treatments currently available.
Depending upon the rate of progression, HRS can be categorized into two types.
Type 1: This is the rapidly progressive type in which the serum creatinine level is found to rise to double the normal (i.e., greater than 221 μmol/L) in less than 2 weeks. The rate of glomerular filtration in this type of patients is very low and the prognosis is poor. Normally, it is connected with a sudden catastrophic event such as SBP (spontaneous bacterial peritonitis) or variceal bleed.
Type 2: This type occurs as a steady decline in the function of the kidneys, and it is associated with refractory ascites and sodium retention.
The main cause of this syndrome is chronic liver disease. Patients suffering from cirrhosis of liver, liver failure, or alcoholic hepatitis are at a high risk of developing this syndrome.
The hepatorenal syndrome is characterized by a range of clinical manifestations such as:
HRS is diagnosed by a clinical examination following the patient history, supplemented by various specialized tests. The criteria for diagnosing this disease are according to the International Ascites Club—an organization that promotes research into advanced cirrhosis.
Major criteria for HRS include the presence of advanced hepatic failure with evidence of portal hypertension, a creatinine clearance <40 mL/min, or serum creatinine >133 μmol/L, plasma expansion with albumin, proteinuria without overt uropathy or renal disease, and the absence of other causes of renal damage such as:
Till date, type 1 HRS is considered to be a terminal stage of liver disease, unless liver transplantation is carried out as soon as the patient is diagnosed. Fortunately, new pharmacological treatments are being discovered to improve our knowledge of the pathogenesis. Newer techniques are also being worked out to increase the efficiency of liver transplantation in HRS patients.