Acute Kidney Injury in Patients With Cirrhosis and HRS

Acute Kidney Injury in Patients With Cirrhosis and HRS is a topic covered in the Washington Manual of Medical Therapeutics.

To view the entire topic, please or .

The Washington Manual is an award-winning, complete mobile solution for nurses and students. Look up information on diseases, tests, and procedures; then consult the database with 5,000+ drugs or refer to 65,000+ dictionary terms. Explore these free sample topics:

-- The first section of this topic is shown below --

General Principles

Acute kidney injury (AKI) in decompensated cirrhosis is a common complication. Revised consensus recommendations define AKI as an increase in serum creatinine ≥0.3 mg/dL within 48 hours or a percentage increase of serum creatinine ≥50% from a known or presumed baseline within the prior 7 days. HRS results from severe peripheral vasodilatation, which leads to renal vasoconstriction. The definition of HRS–AKI (type I HRS) is provided in Table 19-5. Common precipitating factors include systemic bacterial infections, SBP, GI hemorrhage, and large-volume paracentesis without volume expansion. HRS is a diagnosis of exclusion.1

Table 19-5: Diagnostic Criteria of HRS–AKI
  • Diagnosis of cirrhosis and ascites
  • Diagnosis of AKI (an increase in serum creatinine ≥ 0.3 mg/dL within 48 h or a percentage increase of serum creatinine ≥ 50% from a known or presumed baseline within the prior 7 d)
    • Stage 1: Increase in serum creatinine ≥ 0.3 mg/dL or an increase ≥1.5- to 2-fold from baseline
    • Stage 2: Increase in serum creatinine >two- to threefold from baseline
    • Stage 3: increase in serum creatinine >threefold from baseline, >4 mg/dL with an acute increase ≥0.3 mg/dL, or initiation of renal replacement therapy
  • No response after 2 consecutive days of diuretic withdrawal and plasma volume expansion with albumin 1 g/kg
  • Absence of shock
  • No current or recent use of nephrotoxic drugs (NSAIDs, aminoglycosides, iodinated contrast media, etc.)
  • No macroscopic signs of structural kidney injury, defined as
    • Absence of proteinuria (>500 mg/d)
    • Absence of microhematuria (>50 RBCs per high-power field)
    • Normal findings on renal ultrasonography

AKI, acute kidney injury; HRS, hepatorenal syndrome; RBC, red blood cell.

Adapted from Angeli P, Gines P, Wong F, et al. Diagnosis and management of acute kidney injury in patients with cirrhosis: revised consensus recommendations of the International Club of Ascites. J Hepatol. 2015;62:968-974.  [PMID:25638527]

-- To view the remaining sections of this topic, please or --

General Principles

Acute kidney injury (AKI) in decompensated cirrhosis is a common complication. Revised consensus recommendations define AKI as an increase in serum creatinine ≥0.3 mg/dL within 48 hours or a percentage increase of serum creatinine ≥50% from a known or presumed baseline within the prior 7 days. HRS results from severe peripheral vasodilatation, which leads to renal vasoconstriction. The definition of HRS–AKI (type I HRS) is provided in Table 19-5. Common precipitating factors include systemic bacterial infections, SBP, GI hemorrhage, and large-volume paracentesis without volume expansion. HRS is a diagnosis of exclusion.1

Table 19-5: Diagnostic Criteria of HRS–AKI
  • Diagnosis of cirrhosis and ascites
  • Diagnosis of AKI (an increase in serum creatinine ≥ 0.3 mg/dL within 48 h or a percentage increase of serum creatinine ≥ 50% from a known or presumed baseline within the prior 7 d)
    • Stage 1: Increase in serum creatinine ≥ 0.3 mg/dL or an increase ≥1.5- to 2-fold from baseline
    • Stage 2: Increase in serum creatinine >two- to threefold from baseline
    • Stage 3: increase in serum creatinine >threefold from baseline, >4 mg/dL with an acute increase ≥0.3 mg/dL, or initiation of renal replacement therapy
  • No response after 2 consecutive days of diuretic withdrawal and plasma volume expansion with albumin 1 g/kg
  • Absence of shock
  • No current or recent use of nephrotoxic drugs (NSAIDs, aminoglycosides, iodinated contrast media, etc.)
  • No macroscopic signs of structural kidney injury, defined as
    • Absence of proteinuria (>500 mg/d)
    • Absence of microhematuria (>50 RBCs per high-power field)
    • Normal findings on renal ultrasonography

AKI, acute kidney injury; HRS, hepatorenal syndrome; RBC, red blood cell.

Adapted from Angeli P, Gines P, Wong F, et al. Diagnosis and management of acute kidney injury in patients with cirrhosis: revised consensus recommendations of the International Club of Ascites. J Hepatol. 2015;62:968-974.  [PMID:25638527]

There's more to see -- the rest of this topic is available only to subscribers.