AKI in Cirrhosis

Table of Contents

Table of Contents

Yilin Zhang, MD
Pending expert review

Objectives

  1. Differentiate hepatorenal syndrome (HRS) from other causes of acute kidney injury (AKI) in cirrhosis. 
  2. Describe the systemic pathophysiology of both compensated and decompensated cirrhosis in terms of kidney perfusion.
  3. Identify initial treatment for hepatorenal syndrome.
  4. Apply the above frameworks through a series of short cases using learner handouts. 

Teaching Instructions

Plan to spend at least 30-60 minutes preparing for this talk by using the Interactive Board for Learning/Preparing and clicking through the graphics animations to become familiar with the flow and content of the talk.  Begin with reviewing the objectives for the session. We recommend progressing in order from the differential to pathophysiology to the diagnosis and treatment of HRS, followed by the practice cases.  However, feel free to skip steps and spend more time on cases, or visa versa. All clickable elements are indicated by a cursor icon as well as with shading around the button. You may navigate between objectives using the key in the top right corner. The entire talk will take about 30-45 minutes to teach. Print out the handout which includes the schematic for the pathophysiology of cirrhosis as well as practice cases.
  • Objective 1 – The first step in the evaluation of AKI in a patient with cirrhosis is to differentiate between pre-renal, intra-renal, and post-renal causes. The vast majority of AKIs are pre-renal causes, which account for > 60% of all AKI in patients with cirrhosis. AKI increases mortality by 2-6 fold in patients with cirrhosis. This evaluation should specifically include evaluation for infection (including a diagnostic paracentesis) and ruling out a GIB. The differential for pre-renal AKI is broad and can be differentiated into those that are volume responsive and those that are not. Click on each of the pre-renal, intrarenal, and post-renal buttons to reveal the prevalence of each kind of AKI. 
  • Objective 2 –  This objective can be optional in some learners, though understanding the pathophysiology of decompensated cirrhosis is helpful in understanding the treatments used for hepatorenal syndrome. Click on each number in the diagram. 
  • Objective 3 
    • Hepatorenal syndrome (HRS) is a form of pre-renal AKI that does not improve with adequate hydration. This can be done with an albumin challenge (1 g/kg/d albumin x 48 h). If there is an improvement in Cr, this is unlikely HRS. If there is no improvement, this suggests HRS.
    • There are two types of hepatorenal syndrome (click of “HRS”) – type I and type II. Type 1 occurs acutely and is associated with a dramatic rise in serum Cr. This has a poor prognosis with survival on the order of 2 weeks. Type II HRS is more common and occurs slowly over weeks.
    • Treatment of hepatorenal syndrome addresses the pathophysiology of decompensated cirrhosis. The only definitive treatment is a liver transplant!! 
      • Albumin is used to increase effective arterial volume (EAV).
      • Vasopressors, such as midodrine and norepinephrine, would address the decrease in vascular tone. Terlipressin is available in other countries but not in the US.
      • A Transjugular intrahepatic portosystemic shunt (TIPS) procedure can result in delayed improvement in kidney function, but many patients with HRS are too ill to qualify for TIPS procedure.
      • Hemodialysis can be used as a bridge to liver transplant in some patients.
  • Cases – After the completion of the talk, review the practice cases.

Estimated time to present: 30-45 minutes

Handouts

Interactive Boards

For Learning

Use for self-directed learning and for preparing to present

For Teaching

Use for Presenting – there is less text and fewer pop-ups

Take Home Points

  1. AKI in patients with cirrhosis is most commonly caused by pre-renal etiologies and very rarely obstructive.
  2. HRS results in a prerenal AKI that does not respond to volume repletion.
  3. Lack of improvement in Cr after a 48 hour albumin challenge is suggestive of HRS.
  4. HRS is treated with volume expansion with albumin, vasoreactive medications (midodrine, octreotide) to raise the MAP. Only definitive treatment is liver transplant.

References

  1. Regner, KR & Singbartl, K. Kidney Injury in Liver Disease. Crit Care Clin2016. 32; 343-355.
  2. Ge, PS & Runyon, BA. Treatment of Patients with Cirrhosis. NEJM. 2016;375:767-77
  3. Liou, IU. Management of end-stage liver disease. Med Clin North Am. 2014 Jan;98(1):119-52.
  4. Sort, P, et al. Effect of Intravenous Albumin on Renal Impairment and Mortality in Patients with Cirrhosis and Spontaneous Bacterial Peritonitis. NEJM. 1999; 341:403-409.
  5. Runyon, BA. Renal Failure in Cirrhosis. NEJM. 2009; 361(13):1279-1290.
Share on facebook
Facebook
Share on twitter
Twitter
Share on linkedin
LinkedIn