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    Hepatorenal Syndrome

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    Aditi Ujjawal
    Hepatorenal syndrome (HRS) is defined as renal dysfunction in patients with advanced liver disease that is not caused by structural kidney disease. It is characterized by intense renal vasoconstriction. There are two types: type 1 is more severe with a doubling of creatinine in 2 weeks and less than 500 mL urine per day, while type 2 is more indolent with ascites resistant to diuretics. HRS results from splanchnic vasodilation and renal vasoconstriction caused by liver cirrhosis and portal hypertension. Treatment involves vasoconstrictors like terlipressin to reverse HRS or dialysis as a bridge to transplantation.

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    Hepatorenal Syndrome

    Uploaded by

    Aditi Ujjawal
    45 views6 pages
    Hepatorenal syndrome (HRS) is defined as renal dysfunction in patients with advanced liver disease that is not caused by structural kidney disease. It is characterized by intense renal vasoconstriction. There are two types: type 1 is more severe with a doubling of creatinine in 2 weeks and less than 500 mL urine per day, while type 2 is more indolent with ascites resistant to diuretics. HRS results from splanchnic vasodilation and renal vasoconstriction caused by liver cirrhosis and portal hypertension. Treatment involves vasoconstrictors like terlipressin to reverse HRS or dialysis as a bridge to transplantation.

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    Quick ppt on HRS

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    Hepatorenal syndrome

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    Hepatorenal syndrome (HRS) is defined as renal dysfunction in patients with advanced liver disease that is not caused by structural kidney disease. It is characterized by intense renal vasoconstriction. There are two types: type 1 is more severe with a doubling of creatinine in 2 weeks and less than 500 mL urine per day, while type 2 is more indolent with ascites resistant to diuretics. HRS results from splanchnic vasodilation and renal vasoconstriction caused by liver cirrhosis and portal hypertension. Treatment involves vasoconstrictors like terlipressin to reverse HRS or dialysis as a bridge to transplantation.

    Copyright:

    © All Rights Reserved
    Download as KEY, PDF, TXT or read online from Scribd
    Download as key, pdf, or txt
    45 views6 pages

    Hepatorenal Syndrome

    Uploaded by

    Aditi Ujjawal
    Hepatorenal syndrome (HRS) is defined as renal dysfunction in patients with advanced liver disease that is not caused by structural kidney disease. It is characterized by intense renal vasoconstriction. There are two types: type 1 is more severe with a doubling of creatinine in 2 weeks and less than 500 mL urine per day, while type 2 is more indolent with ascites resistant to diuretics. HRS results from splanchnic vasodilation and renal vasoconstriction caused by liver cirrhosis and portal hypertension. Treatment involves vasoconstrictors like terlipressin to reverse HRS or dialysis as a bridge to transplantation.

    Copyright:

    © All Rights Reserved
    Download as KEY, PDF, TXT or read online from Scribd
    Download as key, pdf, or txt
    of 6

    Hepatorenal syndrome

    (HRS)
    Definition
    The hepatorenal syndrome is defined as an otherwise unexplained elevation
    in the plasma creatinine concentration in a patient with advanced hepatic
    disease.
    This is due primarily to intense renal vasoconstriction rather than structural
    renal disease.
    1. Type I hepatorenal syndrome is more severe and defined as a doubling of
    serum creatinine and >2.5 within 2 weeks and less than 400-500 mL of urine
    per day.
    2. Type II is a more indolent process associated with ascites resistant to
    diuretics. Both types are associated with low FENa.
    From International Ascites Club 1996.
    Pathophysiologic mechanisms of hepatorenal syndrome (HRS).

    Hani M. Wadei et al. CJASN 2006;1:1066-1079

    Liver cirrhosis with portal HTNNO, prostaglandinssplanchnic vasodilation


    ECVRAAS, ADH, SNS maladaptive renal vasoconstriction
    HRS can be precipitated by are infection (SBP > other), GI bleed, fluid shifts after large
    volume paracentesis, alcohol-related hepatitis
    Diagnosis:
    Must exclude all other diagnoses. Must demonstrate the presence of
    American Association for the Study of Liver Diseases (AASLD) criteria:
    1. Acute or chronic hepatic failure with portal HTN
    2. Creatinine >= 0.3 over 48hrs or >= 50% over 7days
    3. No signs or symptoms of shock
    4. No renal parenchymal disease or obstruction
    5. No recent nephrotoxins
    6. No improvement after diuretic cessation for 2 days and IV albumin trial
    (1g/kg of 25% albumin for 48hrs, maximum dose 100g/d)
    7. No RBCs >= 50/hpf on urinalysis and no proteinuria >500mg/day
    HRS can occur in patients with preexisting chronic kidney disease eg: DM
    nephropathy.
    Available treatment for HRS:
    1. Vasoconstrictors: midodrine (selective alpha-1 agonist and a systemic
    vasoconstrictor), octreotide (somatostatin analog that reduces splanchnic
    vasodilation), norepinephrine/vasopressin in ICU. Combination of albumin,
    midodrine and octreotide used commonly.
    2. Terlipressin is commonly prescribed in the UK. It is a synthetic vasopressin
    analogue with vasoconstrictor activity in the splanchnic and systemic
    vasculature. Used to buy time for acute liver failure to resolve. Per CONFIRM
    trial, 36.2% of patients who received terlipressin plus albumin achieved HRS
    reversal, defined as a SeCr ≤1.5 mg/dL. Serious adverse effects like
    pulmonary edema, mesenteric ischemia and MI.
    3. Role of dialysis: if there was potential reversibility of impaired liver function,
    for example, in patients with alcoholic hepatitis. Used as bridge to transplant
    in the listed population. For non listed sicker pts - GOC discussions.
    4. Definitive Rx: hepatic transplantation. Mortality in this setting is due to
    hepatic encephalopathy or variceal bleeding rather than due to renal injury.
    5. Role of transjugular intrahepatic portosystemic shunt (TIPS) placement: IR
    puts a shunt going from the portal vein to the hepatic vein under fluoroscopic
    guidance; best outcomes with MELD score less than 14; between 15 and 24,
    clinical judgment about the risk of hepatic decompensation; >24 if transplant
    candidate then better to forego TIPS and wait. https://www.mdcalc.com/calc/78/meld-score-
    model-end-stage-liver-disease-12-older
    References
    1. Renal Pathophysiology: The Essentials by Rennke and Denker, 5th ed.
    2. Hepatorenal Syndrome: Pathophysiology and Management. Wade et al.
    CJASN September 2006, 1 (5) 1066-1079.
    3. Prognosis of Patients with Cirrhosis and AKI Who Initiate RRT.
    Allegretti et al. CJASN January 2018, 13 (1) 16-25.
    4. Terlipressin plus Albumin for the Treatment of Type 1 Hepatorenal
    Syndrome. Wong et al. N Engl J Med Mar 2021; 384:818-828.
    5. Real-world treatment patterns and outcomes using terlipressin in 203
    patients with the hepatorenal syndrome. Moore et al. Aliment Pharmacol
    Ther. 2020 Jul; 52(2): 351–358.
    6. Editorial: treating hepatorenal syndrome—a window and the views.
    Authors' reply. Allegretti et al.

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