Hepatorenal Syndrome (HRS)



Definition:

• Functional, potentially reversible kidney impairment.

• Occurs in advanced liver disease: cirrhosis, severe alcoholic hepatitis, or acute liver failure.

• Caused by splanchnic vasodilation → ↓ renal perfusion + ↑ renal vasoconstriction.

• No structural kidney damage: bland urine, no hematuria/proteinuria.



Pathophysiology:

• Portal hypertension → splanchnic vasodilation.

• ↓ Effective arterial volume → RAAS + sympathetic + ADH activation.

• Renal vasoconstriction dominates → ↓ GFR.

• Tubular function preserved despite ↓ perfusion.



Diagnosis (Clinical Criteria):

• ↑ Serum creatinine ≥0.3 mg/dL or ≥50% from baseline in 48h.

• Bland urine (no casts, protein, or blood).

• Normal kidney ultrasound.

• Exclude other AKI causes (esp. ATN, volume depletion).



Classification:

HRS-AKI (formerly Type 1):

• Rapid progression: SCr >2.5 mg/dL in <2 weeks.

• Often oliguric.

• Unresponsive to volume expansion + diuretic withdrawal.

HRS-Non-AKI (formerly Type 2):

• Gradual kidney decline.

• Associated with diuretic-resistant ascites.



Diagnostic Support:

• No improvement after 2 days of IV albumin (1 g/kg/day).

• Urine sodium could be <10 mEq/L.

• No improvement after diuretic withdrawal.



Treatment Overview:

• Definitive: Liver transplantation.

• Medical:

   - Stop diuretics.

   - Salt and water restriction.

   - IV albumin + vasoconstrictors:

      - Preferred: Terlipressin

      - Norepinephrine may be substituted as the vasoconstrictor

      - Alternatives: Midodrine + Octreotide, or IV Norepinephrine (ICU only).

• Treat underlying liver insult (e.g., alcohol, virus).

• Evaluate for transplant early.



Prognosis:

• High mortality without transplant.

• Vasoconstrictor response does not guarantee survival.

• Urgent liver transplant evaluation essential in all cases.



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