Hepatorenal Syndrome

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 a significant decline in renal perfusion due to severe liver disease, based on the classifications from the International Club of Ascites (ICA):
    • Type I HRS:
      • AKI occurring in patients with acute decompensation of cirrhosis
      • Rapidly progressive
      • 90% mortality within 3 mo; 46% inpatient mortality rate
      • Seen with acute liver failure, alcoholic hepatitis, or following spontaneous bacterial peritonitis (SBP) (bacterial infections are considered the most frequent risk factors)
      • Oliguric or anuric at presentation
    • Type II HRS:
      • Now considered by ICA to be non-AKI HRS or HRS-CKD (chronic kidney disease)
      • Slow course of RF, with functional kidney injury >7 d without other causes of kidney disease
      • 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 AKI due to renal vasoconstriction
    • AKI according to 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
  • Current theories on pathophysiology include advanced cirrhosis, which can lead to portal hypertension triggering splanchnic arterial vasodilation, decreasing systemic vascular resistance, leading to an overall decreased effective arterial volume
    • Reflex activation of sympathetic nervous system
    • Activation of renin–angiotensin–aldosterone system (RAAS)
    • Stimulation of numerous vasoactive substances
  • 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:
    • 8–20% at 1st yr, 40% at 5th yr

Etiology

  • Chronic liver disease, especially alcohol-related (cirrhosis, severe alcoholic hepatitis)
  • Fulminate hepatic failure
  • Precipitating factors:
    • Decreased effective blood volume:
      • GI hemorrhage
      • Vigorous diuresis
      • Large-volume paracentesis
    • Use of nephrotoxic agents:
      • NSAIDs
      • Aminoglycoside
    • Sepsis:
      • SBP is the most important risk factor as it leads to a 33% chance of developing RF during that year
      • SBP prophylaxis reduces the chance of developing acute RF, employed after the 2nd incidence of SBP

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