Acute Kidney Injury in Patients With Cirrhosis and HRS
GENERAL PRINCIPLES
Acute kidney injury (AKI) in decompensated cirrhosis is a common complication. Revised consensus recommendations define AKI as an increase in serum creatinine #8805;0.3 mg/dL within 48 hours or a percentage increase of serum creatinine #8805;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.34TABLE 19-5
DIAGNOSTIC CRITERIA OF HRS-AKI
• Diagnosis of cirrhosis and ascites
• Diagnosis of AKI (an increase in serum creatinine #8805; 0.3 mg/dL within 48 h or a percentage increase of serum creatinine #8805; 50% from a known or presumed baseline within the prior 7 d)
î Stage 1: Increase in serum creatinine #8805; 0.3 mg/dL or an increase #8805;1.5- to 2-fold from baseline
î Stage 2: Increase in serum creatinine gt;two- to threefold from baseline
î Stage 3: increase in serum creatinine gt;threefold from baseline, gt;4 mg/dL with an acute increase #8805;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
î Absence of proteinuria (gt;500 mg/d)
î Absence of microhematuria (gt;50 RBCs per high-power field)
î 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.DIAGNOSIS
HRS is observed in cirrhotic patients with ascites, with and without hyponatremia. HRS has been divided into two types.
• Type I HRS is characterized by the acute onset of rapidly progressive renal failure (lt;2 weeks) unresponsive to volume expansion.
• Type II HRS progresses more slowly but relentlessly and often clinically manifests as diureticresistant ascites.
TREATMENT
Medications
Specific medical therapy is only recommended for type I HRS.
• 25% IV albumin at 1 g/kg body weight (max 100 g) for two consecutive days should be given if the cause of AKI is unidentifiable.
• Terlipressin (vasopressin analog) is not FDA approved for use in the US. In a placebo-controlled trial, 34% of patients who received terlipressin had a reversal of their HRS in comparison with 13% who received placebo.35
• SC somatostatin analogs (octreotide) and oral #945;-adrenergic agonist (midodrine) with IV albumin are commonly used regimens for the management of HRS in the US.
• Norepinephrine can be an alternative to terlipressin.
• Renal replacement therapy may be used when liver transplantation is an option.
Nonpharmacologic Therapies
Hemodialysis may be indicated in patients listed for liver transplantation.
Surgical Management
Liver transplantation may be curative. Patients receiving hemodialysis for more than 6 weeks should be considered for liver and kidney transplantation.
Outcome and Prognosis
Without treatment, patients with type I HRS have a poor prognosis, with death occurring within 1-3 months of onset. Patients with type II HRS have a longer median survival.
More on the topic Acute Kidney Injury in Patients With Cirrhosis and HRS:
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