Differential Diagnosis of AKI in Liver Disease

I recently received a consult for a liver patient with Hep B and Hep C with cirrhosis that developed worsening ascites and oliguric AKI I ask the resident if the usual initial evaluation was done and she was unaware of what that was, therefore I decided to briefly touch on the differential diagnosis and evaluation of acute kidney injury in the patient with liver disease.

The Usual Suspects

The most common causes of AKI in patients with liver disease are:

1.) Pre-renal

  • These are patients already on diuretics and commonly on medications such as lactulose and rifaximin and have increased stool output, both of which can contribute to volume depletion.

2.) ATN

  • Most often is ischemic in this patient population.

    This is clinically useful to recognize as these patients are unlikely to respond to diuretics and albumin infusions may exacerbate their volume overload.

3.) Hepatorenal Syndrome

  • A diagnosis of exclusion after intrinsic and pre-renal causes are ruled out. Here are to diagnostic criteria:

1. Presence of cirrhosis and ascites

2. Serum creatinine >1.5 mg/dL (or 133 micromoles/L)

3. No improvement of serum creatinine (decrease equal to or less than 1.5 mg/dL) after at least 48 hours of diuretic withdrawal and volume expansion with albumin (recommended dose: 1 g/kg b.w. per day up to a maximum of 100 grams of albumin/day)

4. Absence of shock

5. No current or recent treatment with nephrotoxic drugs

6. Absence of parenchymal kidney disease as indicated by proteinuria >500 mg/day, microhematuria (>50 RBCs/high power field, and/or abnormal renal ultrasound scanning

The Others

  1. Viral Hepatitis (Hep B or

    Hep C)

    • Typically will have complement consumed. MPGN (seen with Hep C) and Membranous (seen with Hep B)
  2. Cholemic Nephrosis
    • We talked about this before but can see this in patients with bilirubin > 20
  3. Abdominal Compartment Syndrome
    • By definition intra-abdominal pressure (IAP) > 20. Normally measured by bladder pressure.
    • In patients with tense abdomens from severe ascites the abdominal perfusion pressure can decrease and abdominal organs can become hypoperfused.
    • APP = MAP – IAP, with goal APP of 60 mmHg or more. These patient often have low MAPs to start with so increased IAP can easily lead to decreased APP.

-Adrian

 



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