Pathogenesis: Increased NO generation in splanchnic circulation secondary to portal HTN. This causes systemic vasodilation, which reduces PVR and BP, causing renal hypoperfusion. In turn, compensatory mechanisms such as RAAS, SANS and ADH increase water and sodium retention worsen volume overload.
Risk factor: Severe cirrhosis with portal HTN and edema
Precipitating factor: Reduced renal perfusion through GI bleeding, vomiting, sepsis, excessive diuretic usage, spontaneous bacterial peritonitis and NSAID use can precipitate hepatorenal syndrome.
Laboratory data: prerenal azotemia with a BUN/Cr > 20, elevated Cr > 1.5mg/dL and very low urine sodium(<10 mEq/L or FeNa < 1%).
Diagnosis: Important to r/o intrinsic renal pathology(urinalysis without RBC, WBCs, casts, protein), absence of tubular injury and patients often aren’t responsive to IVF, withdrawal of diuretics. Renal function often declines regardless.
Treatment:
- Involves addressing precipitating factors(infection, anemia, hypovolemia, diarrhea, vomiting, diuretic abuse).
- Splanchnic vasoconstrictors: midodrine, octreotide, norepinephrine
- Liver transplant
Q: 2219, 4752
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