Renal Dysfunction

Top tips:

  1. The International Club of Ascites criteria should be applied for the diagnosis of AKI
  2. When patients present with evidence of renal dysfunction the first steps should be an infectious workup, discontinuation of nephrotoxins, and volume correction.
  3. HRS is a clinical diagnosis that requires exclusion of other pre-renal etiologies and intrinsic renal disease. It no longer requires a serum creatinine cut-off. FeNa < 0.1% after volume replacement suggests HRS.
  4. Treatment for HRS should be started promptly as response to treatment declines with worsening renal function.
  5. The usual starting dose of Midodrine is 5 mg PO tid and starting dose of Octreotide is 100 ug sc tid. Doses can be increased after 24 hours if there is no effect on MAP or renal function. Midodrine and Octreotide should be given with intravenous albumin (see dosing below). Octreotide should not be used alone as it can potentially worsen renal injury.

Order panels:

For adults with cirrhosis admitted with renal dysfunction:

Renal Dysfunction Order Panel

For adults with cirrhosis admitted with hepatorenal syndrome:

Hepatorenal Syndrome (HRS) Order Panel

General Cirrhosis Admission and Discharge Order Sets

*Add specific panels to general admission orders as appropriate*

For adults with cirrhosis requiring hospital admission
Cirrhosis Adult Admission Orders

For adults with cirrhosis requiring hospital discharge
Cirrhosis Adult Discharge Orders

Check out the bottom of the page for short videos from Dr. Wong!

Diagnosis

 

Criteria for HRS-AKI (previously known as Type 1 HRS)
  1. Diagnosis of cirrhosis or acute-on-chronic liver failure (see Diagnosis of cirrhosis and Assess Disease Severity pages for more information)
  2. Diagnosis of AKI as per above definition
  3. Absence of hypovolemia (no or partial response after 2 consecutive days of diuretic withdrawal and plasma volume expansion with albumin (1 g/kg of body weight to a maximum of 100 g/d))
  4. Absence of shock
  5. No current or recent use of nephrotoxic drugs or iodinated contrast media.
  6. No signs of structural kidney injury (absence of proteinuria (> 500 mg/d), microhematuria (> 50 red blood cells per high power field).

New nomenclature for additional HRS-NAKI subtypes
Classification Criteria

  • HRS-AKD (previously known as Type 2 HRS)
  • HRS-CKD
  • eGFR <60ml/min per 1.73m2 for <3 months in absence of other (structural) causes. Percent increase in sCr < 50% using the last available value of outpatient sCr within 3 months as the baseline value
  • eGFR <60ml/min per 1.73m2 for ≥ 3 months in absence of other (structural) causes
  • AKD, Acute kidney disease; AKI, acute kidney injury; CKD, chronic kidney disease; eGFR, estimated glomerular filtration rate; HRS, hepatorenal syndrome; sCr, serum creatinine. 

    AKI management

    Pharmacological therapy for HRS

    Dosing of vasoconstrictors and intravenous albumin (both for at least 7 days).
    Consult a liver specialist if they are not already involved.

    AgentDosing
    Octreotide
    PLUS
    Midodrine
    100-200 mcg SC TID
    5 - 15 mg PO TID
    Norepinephrine0.02 to 0.4 mcg/kg/min
    Terlipressin (not in available in Canada)0.5-2.0mg IV every 4-6 hours
    Albumin given with all vasoconstrictors25% albumin. After initial resuscitation, can give 25 grams daily as tolerated. Pulmonary edema can develop with too much albumin. There is no clear stopping rule. We suggest stopping if serum albumin above 40 g/L.

    Consider consulting Nephrology for:

    Guidance adapted from the AKI Adult-Inpatient Provincial Clinical Knowledge Topic AHS

    • A possible diagnosis that may need specialist treatment (e.g. presence of proteinuria or hematuria on urinalysis can suggest kidney vasculitis or glomerulonephritis; white blood cell casts can suggest tubulointerstitial nephritis ; anemia, hypercalcemia and fractures can suggest multiple myeloma)
    • Progressive AKI despite correction of pre-renal and post-renal factors
    • The patient has had a kidney transplant
    • Pre-existing advanced chronic kidney disease, eGFR less than 30 mL/min/1.73m2
    • Complications associated with AKI which may require renal replacement therapy (i.e. dialysis):
      • Hyperkalemia refractory to medical therapy
      • Metabolic acidosis refractory to medical therapy
      • Symptoms or complications of uremia (pericarditis, encephalopathy)
      • Fluid overload causing cardio-respiratory compromise (pulmonary edema)

    Introducing Dr. Wong

    Video 1- Practical tips for diagnosing and managing AKI in outpatients.

    Video 2 - Practical tips for managing AKI in hospitalized patients – how I do it!

    Patient materials:

    You can direct patients to the following:
    Nutrition

      Calculators:

    Use these calculators to help with the diagnosis:

    FeNa calculator

    Downloadable content:

    You can download these to print or view offline:
    EASL Guidelines

    AHS Acute Kidney Injury

    Defining and Classifying HRS

    References:

    This section was adapted from content using the following evidence based resources in combination with expert consensus. The presented information is not intended to replace the independent medical or professional judgment of physicians or other health care providers in the context of individual clinical circumstances to determine a patient’s care.

    Authors: Dr. Neesh Pannu, Dr. Florence Wong, Dr. Rahima Bhanji, Dr. Puneeta Tandon

    References:

    1. EASL Clinical Practice Guidelines for the management of patients with decompensated cirrhosis. J Hepatol 2018 Aug;69(2):406-460 PMID 29653741
    2. News in pathophysiology, definition and classification of hepatorenal syndrome: step beyond the International Club of Ascites (ICA) consensus document. J Hepatol 2019 Oct;71(4):811-822. PMID 31302175
    3. Wong F et al. Midodrine, octreotide, albumin, and TIPS in selected patients with cirrhosis and type 1 hepatorenal syndrome. Hepatology 2004 Jul;40(1):55-64. PMID 15239086
    4. Gines P et al. Hepatorenal syndrome. Nat Rev Dis Primers. 2018 Sep 13;4(1):23. PMID 30213943
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