Hepatorenal syndrome
The hepatorenal syndrome refers to renal failure of unknown etiology that occurs in a fully hydrated patient with severe, often progressive, liver disease. Urine biochemistry is characteristic and renal histopathology unremarkable.
The pathogenesis of the hepatorenal syndrome appears to involve intense intrarenal vasoconstriction and alteration in renal cortical blood flow, possibly due to an imbalance of prostaglandins and thromboxane. Early clinical experience suggested that only orthotopic liver transplantation was able to reverse the hepatorenal syndrome, although more recent evidence has reported up to 50 per cent survival in hepatorenal failure following paracetamol (acetaminophen) overdose. Renal failure is reversed after liver transplantation, suggesting that it is due to circulating or systemic factors. Excessive use of diuretics, sepsis, abdominal paracentesis, and gastrointestinal hemorrhage are all associated with an increased risk of the hepatorenal syndrome and suggest a functional etiology.
Clinical presentation
Typically, patients who develop the hepatorenal syndrome have signs of advanced liver disease, such as icterus, ascites, palmar erythema, spider angiomas, and hepatic encephalopathy. Laboratory findings confirm hepatic failure, with elevated serum bilirubin, liver enzymes, and ammonia. The impaired synthetic function of the liver usually results in hypoalbuminaemia and prolongation of the prothrombin time. Hyponatraemia, hypokalaemia, and alkalosis are common accompaniments. Hyponatraemia results from proximal tubular reabsorption of sodium and water with non-osmotic release of vasopressin. The first sign of hepatorenal syndrome is usually oliguria. The major differential diagnoses include prerenal azotaemia and vasomotor nephropathy (acute tubular necrosis). The patient with hepatorenal syndrome appears well hydrated and volume depletion can usually be excluded.
The FENa is less than 1 per cent and the urinary sodium less than 10 to 15 mmol/1, in contrast to vasomotor nephropathy, which characteristically has a high urinary sodium content—over 30 mmol/1. If prerenal azotaemia is suspected, a cautious fluid challenge consisting of about 250 ml of crystalloid or colloid infused over 30 min can be tried. If doubt remains about the volume status of the patient, a flow-directed pulmonary arterial catheter should be inserted for accurate assessment of left heart filling pressures.
The urine sediment should be examined carefully. The presence of cellular casts suggests vasomotor nephropathy rather than hepatorenal syndrome. Obstructive uropathy should be excluded by renal ultrasonography or, if necessary, retrograde pyelography.
Treatment
When treating any patient with advanced liver disease, it is essential to avoid factors that precipitate the hepatorenal syndrome. Adequate nutrition must be maintained and electrolyte abnormalities corrected. Diuretics should be used judiciously and ascites drained only for specific indications. Any intercurrent infection must be treated aggressively. The use of certain drugs, such as the non-steroidal anti-inflammatory agents, angiotensin-converting enzyme inhibitors and tetracyclines, should be avoided, and aminoglycosides should not be used unless this is unavoidable.
There is currently no specific treatment for the hepatorenal syndrome; therapy is directed at supporting the underlying liver disease. Haemodialysis and haemofiltration may control the metabolic disturbances of renal failure but the outcome is determined by the degree of liver impairment.
Pharmacological agents that have been used in an attempt to reverse the hepatorenal syndrome include dopamine, isoprenaline, phenoxybenzamine, phentolamine, aminophylline, mannitol, metaraminol, adrenaline (epinephrine), papaverine, and prostaglandin A1. All have been without effect in double-blind studies. Recovery of renal function has occurred following peritoneojugular (LaVeen) and portacaval shunting. Orthotopic liver transplantation appears to offer the best hope for reversal of the hepatorenal syndrome but is only available for a relatively small group of suitable patients.
The hepatorenal syndrome refers to renal failure of unknown etiology that occurs in a fully hydrated patient with severe, often progressive, liver disease. Urine biochemistry is characteristic and renal histopathology unremarkable.
The pathogenesis of the hepatorenal syndrome appears to involve intense intrarenal vasoconstriction and alteration in renal cortical blood flow, possibly due to an imbalance of prostaglandins and thromboxane. Early clinical experience suggested that only orthotopic liver transplantation was able to reverse the hepatorenal syndrome, although more recent evidence has reported up to 50 per cent survival in hepatorenal failure following paracetamol (acetaminophen) overdose. Renal failure is reversed after liver transplantation, suggesting that it is due to circulating or systemic factors. Excessive use of diuretics, sepsis, abdominal paracentesis, and gastrointestinal hemorrhage are all associated with an increased risk of the hepatorenal syndrome and suggest a functional etiology.
Clinical presentation
Typically, patients who develop the hepatorenal syndrome have signs of advanced liver disease, such as icterus, ascites, palmar erythema, spider angiomas, and hepatic encephalopathy. Laboratory findings confirm hepatic failure, with elevated serum bilirubin, liver enzymes, and ammonia. The impaired synthetic function of the liver usually results in hypoalbuminaemia and prolongation of the prothrombin time. Hyponatraemia, hypokalaemia, and alkalosis are common accompaniments. Hyponatraemia results from proximal tubular reabsorption of sodium and water with non-osmotic release of vasopressin. The first sign of hepatorenal syndrome is usually oliguria. The major differential diagnoses include prerenal azotaemia and vasomotor nephropathy (acute tubular necrosis). The patient with hepatorenal syndrome appears well hydrated and volume depletion can usually be excluded.
The FENa is less than 1 per cent and the urinary sodium less than 10 to 15 mmol/1, in contrast to vasomotor nephropathy, which characteristically has a high urinary sodium content—over 30 mmol/1. If prerenal azotaemia is suspected, a cautious fluid challenge consisting of about 250 ml of crystalloid or colloid infused over 30 min can be tried. If doubt remains about the volume status of the patient, a flow-directed pulmonary arterial catheter should be inserted for accurate assessment of left heart filling pressures.
The urine sediment should be examined carefully. The presence of cellular casts suggests vasomotor nephropathy rather than hepatorenal syndrome. Obstructive uropathy should be excluded by renal ultrasonography or, if necessary, retrograde pyelography.
Treatment
When treating any patient with advanced liver disease, it is essential to avoid factors that precipitate the hepatorenal syndrome. Adequate nutrition must be maintained and electrolyte abnormalities corrected. Diuretics should be used judiciously and ascites drained only for specific indications. Any intercurrent infection must be treated aggressively. The use of certain drugs, such as the non-steroidal anti-inflammatory agents, angiotensin-converting enzyme inhibitors and tetracyclines, should be avoided, and aminoglycosides should not be used unless this is unavoidable.
There is currently no specific treatment for the hepatorenal syndrome; therapy is directed at supporting the underlying liver disease. Haemodialysis and haemofiltration may control the metabolic disturbances of renal failure but the outcome is determined by the degree of liver impairment.
Pharmacological agents that have been used in an attempt to reverse the hepatorenal syndrome include dopamine, isoprenaline, phenoxybenzamine, phentolamine, aminophylline, mannitol, metaraminol, adrenaline (epinephrine), papaverine, and prostaglandin A1. All have been without effect in double-blind studies. Recovery of renal function has occurred following peritoneojugular (LaVeen) and portacaval shunting. Orthotopic liver transplantation appears to offer the best hope for reversal of the hepatorenal syndrome but is only available for a relatively small group of suitable patients.
Comments
keep it up nice work...