Hepatorenal Syndrome - Diagnosis

Diagnosis

There can be many causes of kidney failure in individuals with cirrhosis or fulminant liver failure. Consequently, it is a challenge to distinguish hepatorenal syndrome from other entities that cause renal failure in the setting of advanced liver disease. As a result, additional major and minor criteria have been developed to assist in the diagnosis of hepatorenal syndrome.

The major criteria include liver disease with portal hypertension; renal failure; the absence of shock, infection, recent treatment with medications that affect the function of the kidney (nephrotoxins), and fluid losses; the absence of sustained improvement in renal function despite treatment with 1.5 litres of intravenous normal saline; the absence of proteinuria (protein in the urine); and, the absence of renal disease or obstruction of renal outflow as seen on ultrasound.

The minor criteria are the following: a low urine volume (less than 500 mL (18 imp fl oz; 17 US fl oz) per day), low sodium concentration in the urine, a urine osmolality that is greater than that in the blood, the absence of red blood cells in the urine, and a serum sodium concentration of less than 130 mmol/L.

Many other diseases of the kidney are associated with liver disease and must be excluded before making a diagnosis of hepatorenal syndrome. Individuals with pre-renal failure do not have damage to the kidneys, but as in individuals with HRS, have renal dysfunction due to decreased blood flow to the kidneys. Also, similarly to HRS, pre-renal failure causes the formation of urine that has a very low sodium concentration. In contrast to HRS, however, pre-renal failure usually responds to treatment with intravenous fluids, resulting in reduction in serum creatinine and increased excretion of sodium. Acute tubular necrosis (ATN) involves damage to the tubules of the kidney, and can be a complication in individuals with cirrhosis, because of exposure to toxic medications or the development of decreased blood pressure. Because of the damage to the tubules, ATN affected kidneys usually are unable to maximally resorb sodium from the urine. As a result, ATN can be distinguished from HRS on the basis of laboratory testing, as individuals with ATN will have urine sodium measurements that are much higher than in HRS; however, this may not always be the case in cirrhotics. Individuals with ATN also may have evidence of hyaline casts or muddy-brown casts in the urine on microscopy, whereas the urine of individuals with HRS is typically devoid of cellular material, as the kidneys have not been directly injured. Some viral infections of the liver, including hepatitis B and hepatitis C can also lead to inflammation of the glomerulus of the kidney. Other causes of renal failure in individuals with liver disease include drug toxicity (notably the antibiotic gentamicin) or contrast nephropathy, caused by intravenous administration of contrast agents used for medical imaging tests.