Hepatorenal syndrome

Pathophysiology

  • important complication of end stage liver disease
  • liver: cirrhosis => increased intrahepatic vascular resistance => portal HTN => increase NO, vasodilators => splanchnic arterial dilation (celiac, superior mesenteric, and inferior mesenteric arteries) => hypotension
  • kidney: decrease in renal perfusion => activates RAAS/vasopressin => renal vasoconstriction with decreased perfusion and glomerular filtration.

Triggers:

  • Decreased perfusion/volume:
    • GI bleed, sepsis, vomiting, diuretic use, NSAID use
    • ascites
    • too much lactulose
  • SBP

Diagnosis

  • decreased renal perfusion (decrease in GFR) without another clear cause
    • Cr > 1.5
    • BUN:Cr elevated > 20:1
  • no tubular injury: no RBC, protein, granular casts in urine
    • protein excretion < 500 mg/d
  • no obstruction: US benign
  • Hyponatremia (dilutional hyponatremia)
    • low Na excretion in urine (<10 mmol/L)
  • lack of improvement with volume resuscitation (BUN:Cr could be high in either prerenal or hepatorenal)
  • look for triggers: paracentesis if has ascites

Treatment

  • Goal: increase MAP > 82 (raise map by 10)
  • Address triggers (hypovolemia, anemia, infection)
  • Limit diuretics, beta blocker
  • Plasma expander albumin
    • IV bolus (1g/kg per day, up to 100g max) on 1st day
    • followed by 25-50g/day until midodrine/octreotide discontinued
    • continue 2-3 days
  • Splanchnic vasoconstrictors
    • midodrine (alpha agonist): 7.5 mg, titrate q8h up to 15 mg TID
    • octreotide (inhibits vasodilation): gtt 50 mcg/hr or 100-200 mcg SQ q8h
    • norepinephrine
  • Increase urine output to at least 200 cc/4 hours
  • TIPS
  • discontinue therapy if no response after 4 days
  • dialysis/transplant is next option
  • Liver transplant
  • Dialysis may be attempted to help bridge to liver transplantation.