Today in morning report we heard about a patient with decompensated liver disease. He presented with jaundice and an elevated creatinine.
When patients with cirrhosis present with an AKI, we ask is this Hepatorenal syndrome or something else?
Things that can trigger renal failure in cirrhotic patients:
- Overdiuresis
- Overdiuresis
- NSAIDs (cirrhotic patients very dependent on renal prostaglandin synthesis) and other nephrotoxins
- GI bleed
- Bacterial infections including translocation of bacteria in gut and spontaneous bacterial peritonitis (SBP)
- Any acute decompensation of cirrhosis
- GI bleed
- Bacterial infections including translocation of bacteria in gut and spontaneous bacterial peritonitis (SBP)
- Any acute decompensation of cirrhosis
Type 1: Develops rapidly. Creatinine doubling over less than 2 week period
Type 2: More gradual than type 1.
To be labelled hepatorenal syndrome:
- no improvement after 2 days off diuretics and albumin 1gm/kg/day for 2days minimum
- no recent nephrotoxic drugs
- no shock
- no evidence of renal parenchymal disease (significant proteinuria, hematuria, or abnormal looking kidneys on ultrasound)
- no improvement after 2 days off diuretics and albumin 1gm/kg/day for 2days minimum
- no recent nephrotoxic drugs
- no shock
- no evidence of renal parenchymal disease (significant proteinuria, hematuria, or abnormal looking kidneys on ultrasound)
Initial Management of AKI in patient with ascites:
- Exclude bacterial infection: diagnostic paracentesis + other cultures
- Exclude GI bleed
- Hold diuretics
- Stop nephrotoxic drugs
- give a trial of albumin as above
Distinguishing hepatorenal syndrome from ATN can be tricky as both can cause the presence of heme granular casts in the urine. Once diuretics are held, a FENa (fractional excretion of sodium) less than 1% supports the diagnosis of hepatorenal syndrome.
Specific therapies for hepatorenal syndrome:
- Terlipressin: improves renal function, no effect on survival found so far
- Midodrine and octreotide together: small studies suggest benefit on renal function
Distinguishing hepatorenal syndrome from ATN can be tricky as both can cause the presence of heme granular casts in the urine. Once diuretics are held, a FENa (fractional excretion of sodium) less than 1% supports the diagnosis of hepatorenal syndrome.
Specific therapies for hepatorenal syndrome:
- Terlipressin: improves renal function, no effect on survival found so far
- Midodrine and octreotide together: small studies suggest benefit on renal function
- TIPS= transjugular intrahepatic portosystemic shunt: some observational studies show improvement, however many patients with HRS too sick to undergo this procedure
- Liver transplantation- don't forget to consider this
Prognosis of HRS is very poor. Mortality is higher with type 1 hepatorenal syndrome than with type 2 (median survival, 1 month vs. 6 months)
Prevention of HRS in patients with ascites:
- Albumin as part of treatment for SBP: 1.5 gm/kg at initiation and 1gm/kg at 48 hours.
- Prevention of SBP with norfloxacin in selected patients- see this study
Here is a link to the most recent NEJM review on the topic
Prognosis of HRS is very poor. Mortality is higher with type 1 hepatorenal syndrome than with type 2 (median survival, 1 month vs. 6 months)
Prevention of HRS in patients with ascites:
- Albumin as part of treatment for SBP: 1.5 gm/kg at initiation and 1gm/kg at 48 hours.
- Prevention of SBP with norfloxacin in selected patients- see this study
Here is a link to the most recent NEJM review on the topic
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