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.
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