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
- 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
- Decreased effective blood volume:
-- To view the remaining sections of this topic, please log in or purchase a subscription --
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
- 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
- Decreased effective blood volume:
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