Internal Medicine · Year 3 · from Internal Medicine

Case 3: Hepatorenal Syndrome

Patient Presentation

A 55-year-old man with alcohol-related cirrhosis (Child-Pugh C) presents with oliguria for 2 days. He was recently hospitalized for SBP and completed antibiotic treatment 1 week ago. He has refractory ascites requiring weekly paracenteses. He denies diarrhea, vomiting, or NSAID use. He has been compliant with his medications.

Vital Signs

  • Blood Pressure: 92/58 mmHg
  • Heart Rate: 96 bpm
  • Respiratory Rate: 18/min
  • Oxygen Saturation: 96% on room air

Physical Examination

  • General: Cachectic, jaundiced
  • Cardiovascular: Hypotensive, no JVD
  • Abdomen: Tense ascites
  • Extremities: Minimal edema (third-spacing)
  • Skin: Multiple spider angiomata

Laboratory Results

  • Creatinine: 3.2 mg/dL (was 1.2 two weeks ago)
  • Sodium: 124 mEq/L
  • BUN: 58 mg/dL
  • Urinalysis: Bland (no casts, no protein, SG 1.020)
  • Urine sodium: 6 mEq/L
  • Urine output: 250 mL in 24 hours

Clinical Image

Figure 3: Diagram illustrating the pathophysiology of hepatorenal syndrome: splanchnic vasodilation leads to decreased effective arterial blood volume, activating vasoconstrictors that cause renal vasoconstriction.

Image Source: Educational illustration for teaching purposes.

Questions

  1. What defines hepatorenal syndrome-acute kidney injury (HRS-AKI)?
  • A) Any AKI in a cirrhotic patient
  • B) AKI in cirrhosis without improvement after diuretic withdrawal and volume expansion, no shock, no nephrotoxin exposure, no parenchymal kidney disease
  • C) Creatinine >2 mg/dL
  • D) Oliguria alone
  1. What should be the initial diagnostic and therapeutic approach to AKI in cirrhosis?
  • A) Immediate dialysis
  • B) Hold diuretics, volume expand with albumin (1 g/kg x 2 days), rule out other causes
  • C) Start vasoconstrictors immediately
  • D) Liver transplant evaluation only
  1. What is the treatment for HRS-AKI?
  • A) Diuretics
  • B) Albumin plus vasoconstrictors (terlipressin, norepinephrine, or midodrine + octreotide)
  • C) NSAIDs
  • D) Fluid restriction only
  1. What is the prognosis of HRS-AKI and what is the definitive treatment?
  1. How is HRS differentiated from other causes of AKI in cirrhosis?

Answers

  1. B) AKI in cirrhosis without improvement after diuretic withdrawal and volume expansion, no shock, no nephrotoxin exposure, no parenchymal kidney disease - HRS-AKI criteria (revised 2015):
  • Cirrhosis with ascites
  • AKI (creatinine increase ≥0.3 mg/dL or ≥50%)
  • No improvement after diuretic withdrawal and albumin challenge (1 g/kg x 2 days)
  • Absence of shock, nephrotoxins (NSAIDs, aminoglycosides, contrast)
  • No evidence of parenchymal kidney disease (proteinuria <500 mg/day, normal urine sediment, no obstruction)
  1. B) Hold diuretics, volume expand with albumin (1 g/kg x 2 days), rule out other causes - Initial approach:
  • Stop diuretics and nephrotoxins
  • Albumin 1 g/kg (max 100 g) for 2 consecutive days
  • Assess response at 48 hours
  • If no improvement, likely HRS - start vasoconstrictor therapy
  • Check urinalysis to exclude parenchymal disease
  • Rule out obstruction (renal ultrasound)
  1. B) Albumin plus vasoconstrictors (terlipressin, norepinephrine, or midodrine + octreotide) - Treatment regimens:
  • First-line: Terlipressin + albumin (not available in US until recently)
  • Alternative: Norepinephrine + albumin (ICU setting)
  • Alternative: Midodrine (7.5-15 mg TID) + octreotide (100-200 mcg TID) + albumin (non-ICU)
  • Albumin: 20-40 g/day
  • Continue until creatinine <1.5 mg/dL or max 14 days
  1. Prognosis and definitive treatment:
  • HRS-AKI has very poor prognosis: median survival weeks to months without intervention
  • Response to medical therapy: 40-50% with terlipressin, lower with other regimens
  • Definitive treatment: Liver transplantation
  • HRS patients receive MELD exception points for transplant prioritization
  • TIPS may be considered as bridge to transplant in select cases
  • RRT may be needed as bridge to transplant but does not treat underlying HRS
  1. Differentiating HRS from other AKI causes in cirrhosis:
  • Prerenal (hypovolemia): Responds to volume expansion
  • ATN: Muddy brown casts, FENa >2%, granular casts (HRS has bland sediment, FENa <1%)
  • Drug-induced: Recent nephrotoxin exposure
  • Post-renal: Obstruction on imaging
  • Parenchymal disease: Proteinuria, hematuria, abnormal sediment
  • HRS = diagnosis of exclusion after ruling out other causes and no response to albumin

Learning Points

  1. SAAG ≥1.1 g/dL indicates portal hypertension; diagnostic paracentesis is essential for new-onset or worsening ascites.
  1. SBP is diagnosed by ascitic fluid PMN ≥250/μL; treatment is ceftriaxone plus albumin; prophylaxis indicated for high-risk patients.
  1. Hepatic encephalopathy is treated with lactulose (titrate to 2-3 stools/day); rifaximin added for recurrence; protein restriction is NOT recommended.
  1. HRS-AKI is diagnosed after excluding other AKI causes and no response to albumin challenge; treatment includes vasoconstrictors plus albumin.
  1. Liver transplant evaluation is essential for patients with decompensated cirrhosis (ascites, HE, variceal bleeding, HRS).

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