Hepatorenal Syndrome

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Basics

Description

  • Renal failure (RF) in patients with acute or chronic liver disease with no other identifiable cause of renal pathology
  • Hepatorenal syndrome (HRS) represents significant decline in renal perfusion due to severe liver disease:
    • Type I HRS:
      • Acute form with spontaneous RF in patients with liver disease
      • Rapidly progressive
      • 90% mortality within 3 mo
      • Seen with acute liver failure or alcoholic hepatitis
      • Oliguric or anuric at presentation
    • Type II HRS:
      • Slow course of RF
      • Seen in patients with diuretic resistant ascites
      • Lower mortality than type I HRS
  • Hallmarks of HRS:
    • Patients must have cirrhosis and ascites
    • Prerenal disease
    • A functional form of acute kidney injury (AKI) due to renal vasoconstriction
    • AKI according to International Club of Ascites (ICA) criteria
    • Reversible renal vasoconstriction and mild systemic hypotension, but without shock
    • Kidneys have normal histology and structure on US
    • Lack of improvement in renal function after volume expansion with albumin and diuretic withdrawal for 48 hr
    • No current use of nephrotoxic drugs
  • Liver disease causes systemic vasodilation with decrease in arterial blood volume:
    • Reflex activation of sympathetic nervous system
    • Activation of renin–angiotensin–aldosterone system (RAAS)
    • Stimulation of numerous vasoactive substances:
      • Nitric oxide
      • Prostacyclin
      • Atrial natriuretic peptide (ANP)
      • Arachidonic acid metabolites
      • Platelet-activating factor
      • Endothelins
      • Catecholamines
      • Angiotensin II
      • Thromboxane
  • Action of vasoconstrictors prevails over vasodilator effects:
    • Renal hypoperfusion ensues due to renal cortical vasoconstriction
    • Decrease in renal blood flow and glomerular filtration rates (GFRs)
  • Decreased urine sodium excretion (U Na <10 mEq/d)
  • Incidence of HRS:
    • 18% at first year, 39% at 5 yr
  • Hyponatremia and high plasma renin levels are risk factors

Etiology

  • Chronic liver disease, especially alcohol related (cirrhosis, severe alcoholic hepatitis)
  • Fulminate hepatic failure
  • Precipitating factors:
    • Decreased effective blood volume:
      • GI bleeding
      • Vigorous diuresis
      • Large-volume paracentesis
    • Use of nephrotoxic agent:
      • NSAIDs
      • Aminoglycoside
    • Sepsis:
      • Spontaneous bacterial peritonitis (SBP) leads to a 33% chance of developing RF during that year
      • SBP prophylaxis reduces the chance of developing acute RF

-- To view the remaining sections of this topic, please or --

Basics

Description

  • Renal failure (RF) in patients with acute or chronic liver disease with no other identifiable cause of renal pathology
  • Hepatorenal syndrome (HRS) represents significant decline in renal perfusion due to severe liver disease:
    • Type I HRS:
      • Acute form with spontaneous RF in patients with liver disease
      • Rapidly progressive
      • 90% mortality within 3 mo
      • Seen with acute liver failure or alcoholic hepatitis
      • Oliguric or anuric at presentation
    • Type II HRS:
      • Slow course of RF
      • Seen in patients with diuretic resistant ascites
      • Lower mortality than type I HRS
  • Hallmarks of HRS:
    • Patients must have cirrhosis and ascites
    • Prerenal disease
    • A functional form of acute kidney injury (AKI) due to renal vasoconstriction
    • AKI according to International Club of Ascites (ICA) criteria
    • Reversible renal vasoconstriction and mild systemic hypotension, but without shock
    • Kidneys have normal histology and structure on US
    • Lack of improvement in renal function after volume expansion with albumin and diuretic withdrawal for 48 hr
    • No current use of nephrotoxic drugs
  • Liver disease causes systemic vasodilation with decrease in arterial blood volume:
    • Reflex activation of sympathetic nervous system
    • Activation of renin–angiotensin–aldosterone system (RAAS)
    • Stimulation of numerous vasoactive substances:
      • Nitric oxide
      • Prostacyclin
      • Atrial natriuretic peptide (ANP)
      • Arachidonic acid metabolites
      • Platelet-activating factor
      • Endothelins
      • Catecholamines
      • Angiotensin II
      • Thromboxane
  • Action of vasoconstrictors prevails over vasodilator effects:
    • Renal hypoperfusion ensues due to renal cortical vasoconstriction
    • Decrease in renal blood flow and glomerular filtration rates (GFRs)
  • Decreased urine sodium excretion (U Na <10 mEq/d)
  • Incidence of HRS:
    • 18% at first year, 39% at 5 yr
  • Hyponatremia and high plasma renin levels are risk factors

Etiology

  • Chronic liver disease, especially alcohol related (cirrhosis, severe alcoholic hepatitis)
  • Fulminate hepatic failure
  • Precipitating factors:
    • Decreased effective blood volume:
      • GI bleeding
      • Vigorous diuresis
      • Large-volume paracentesis
    • Use of nephrotoxic agent:
      • NSAIDs
      • Aminoglycoside
    • Sepsis:
      • Spontaneous bacterial peritonitis (SBP) leads to a 33% chance of developing RF during that year
      • SBP prophylaxis reduces the chance of developing acute RF

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