Reversal of Hepatorenal Syndrome With the Use of Fix Doses of Vasoconstrictors and Albumin

Abstract

INTRODUCTION: Hepatorenal syndrome (HRS) is a serious complication of advanced liver cirrhosis; carries a grim prognosis with 2-week mortality rate as high as 80% in untreated type 1 HRS. We present a patient with type 1 HRS where the renal failure resolved with the use of norepinephrine and albumin infusion. CASE PRESENTATION: 42-year-old-man with advanced hepatitis C and liver cirrhosis (Child’s C, MELD score 38), was admitted to ICU with acute renal failure. Examination revealed an alert and oriented male, in mild distress with massive anasarca; blood pressure 100/60mmHg, respiratory rate 20/min. Laboratory: albumin 1.5g/dl, elevated AST, ALT, bilirubin and serum creatinine (SCr) 2.8mg/dl. He was anuric during the first 12 hours of admission. Urine analysis demonstrated normal sediment, urine sodium 31mEq/L and FENA 0.3%. His SCr was 0.8mg/dl two-months prior. He had not received nephrotoxic medications or diuretics; post-renal obstruction was excluded with a bladder catheter. Abdominal paracentesis and abdomino-pelvic ultrasound were noncontributory. Central venous pressure was 6 cmH2O and intra-abdominal pressure was 4 cmH2O. Intravenous saline and albumin were started. Patient remained anuric with worsening of creatinine (4.6mg/dl) which favored diagnostic of HRS type 1. Infusion of norepinephrine (5ug/kg/ml ) and albumin (1g/kg) were initiated on third day of admission resulting in an increase in urine output and improvement in renal function. Infusions were discontinued on day six (SCr 0.6mg/dL). Two weeks later renal function remains normal. DISCUSSION: HRS is defined as SCr of >1.5 mg/dl, not reduced with administration of albumin and discontinuation of diuretics. Need to exclude use of nephrotoxic drugs, presence of shock, hypovolemia, peritonitis and parenchymal renal disease. HRS is classified into type 1 (doubling of SCr to >2.5 mg/dl in <2 weeks) and type 2 (gradual increase in SCr to>1.5 mg/dl). HRS is characterized by functional renal vasoconstriction, peripheral vasodilatation and pooling of blood in splanchnic circulation leading to severe reduction in GFR with minimal renal histologic abnormalities. Therapeutic management includes administration of vasoconstrictors. Vasopressin analogues (terlipressin-approved in Europe) are effective in 40-50% of patients. Midodrine and norepinephrine, two α1-adrenergic receptor agonists have been shown to be effective. Liver transplantation is the ultimate treatment for HRS, but vasoconstrictors, TIPS, and/or RRT can be utilized as a bridge to transplantation. CONCLUSIONS: HRS is a severe complication of liver cirrhosis. Identifying the specific type of renal failure in cirrhosis has prognostic and therapeutic implications. The use of vasoconstrictors should be considered early in the management of HRS.