A complication of cirrhosis with avid sodium retention with dilutional hyponatremia and activation of the renin-angiogenesis system, with ineffective arterial blood flow because of splanchnic vasodilation.
With progressive disease renal vasoconstriction occurs leading to reduction in renal blood flow and glomerular filtration rates.
When considering a liver transplantation for cirrhosis renal failure is one of the most important risk factors.
Cirrhosis and renal failure patients are at high risk for death while awaiting liver transplantation with increased frequency of complications and reduced survival after transplantation compared to individuals without renal failure.
The MELD score has increased the number of patients with renal failure that receive a liver transplant and it has reduced mortality rate among patients awaiting liver transplant.
Renal failure in cirrhosis primarily related to circulatory changes, a reduction in systemic vascular resistance due t primary arterial vasodilation in the splanchnic circulation as a result of portal hypertension.
Arterial vasodilation in portal hypertension related to nitrous oxide, carbon monoxide and endogenous cannabinoids found mainly in the splanchnic circulation.
In early cirrhosis with moderate portal hypertension increased cardiac output compensates for modest reductions in systemic vascular resistance allowing arterial pressure and arterial blood volume to remain in the normal range.
Use of nonsteroidal anti-inflammatory (NSAIDs) drugs can precipitate the process.
Can be precipitated by progeny agents, overuse of diuretics, volume depletion, large volume paracentesis for ascites, spontaneous bacterial peritonitis and sepsis.
Diagnostic criteria include: serum creatinine greater than 1.5 mg/dL, exclusion of shock, volume depletion, bacterial infection, and nephrotoxic drugs, failure to improve with improving fluid volume in the presence of prior diuretics or volume depletion, no evidence of proteinuria, urinary obstruction or parenchyma renal disease.
Two types of clinical hepatorenal syndrome, types I and type II.
Type I is associated with a decrease of more than 50% in creatinine clearance to less than 20 cc/minute or a doubling of the creatinine level to more than 2.5 mg/dL in 2 weeks time.
Prognosis for type I is poor with 80% mortality within 2 weeks following diagnosis.
Type II can evolve into type I.
In type II renal deterioration is not as severe as in type I disease and manifests as refractory ascites with a six months survival of 50% at 6 months.
Broad spectrum antibiotics utilized with the diagnosis.
Liver transplantation provides the most successful treatment with a survival rate of more than 80% over 1 year.
Albumin infusions with arterial vasoconstrictors can be utilized for type I process.
Midodrine (ProAmatine) with octreotide may improve renal function in patients with type I disease.
Terlipressin an analogue of vasopressin can increase the glomerular filtration rate in up to 75% of the patients.
TIPPS can improve creatinine clearance in this situation.