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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