Does prerenal Acute Kidney Injury (AKI) rule out Hepatorenal Syndrome (HRS)?

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Last updated: May 7, 2025 • View editorial policy

From the Guidelines

No, a prerenal acute kidney injury (AKI) does not rule out hepatorenal syndrome (HRS). In fact, HRS is a specific form of prerenal AKI that occurs in patients with advanced liver disease and portal hypertension. HRS is characterized by intense renal vasoconstriction and reduced renal blood flow in the absence of other identifiable causes of kidney injury. To diagnose HRS, several criteria must be met, including the presence of cirrhosis with ascites, serum creatinine >1.5 mg/dL, no improvement in kidney function after at least 2 days of diuretic withdrawal and volume expansion with albumin, absence of shock, no recent use of nephrotoxic drugs, and absence of parenchymal kidney disease 1.

Key Considerations

  • The management of HRS typically involves vasoconstrictors like terlipressin or norepinephrine combined with albumin to improve effective arterial blood volume and renal perfusion 1.
  • The use of IV albumin is recommended as the volume expander of choice in hospitalized patients with cirrhosis and ascites presenting with AKI, at a dose of 1 g/kg of body weight daily for 2 consecutive days (with a cap of 100 g/d) 1.
  • Vasoactive drugs (terlipressin, NE, or combination of octreotide/midodrine) should be used in the treatment of HRS-AKI but not in other forms of AKI in cirrhosis 1.
  • The definitive treatment for HRS is liver transplantation, as the kidney dysfunction is a consequence of the liver disease and often improves when liver function is restored.

Diagnostic Approach

  • A trial of volume expansion with albumin is recommended to differentiate between prerenal AKI and HRS-AKI 1.
  • Lack of response to volume expansion with albumin is one of the diagnostic criteria of HRS-AKI 1.
  • The diagnostic criteria for HRS include the presence of cirrhosis with ascites, serum creatinine >1.5 mg/dL, no improvement in kidney function after at least 2 days of diuretic withdrawal and volume expansion with albumin, absence of shock, no recent use of nephrotoxic drugs, and absence of parenchymal kidney disease 2, 3.

Treatment Approach

  • The treatment of HRS typically involves a combination of vasoconstrictors and albumin to improve effective arterial blood volume and renal perfusion. The choice of vasoconstrictor and the dose of albumin should be individualized based on the patient's volume status and response to treatment 1.
  • The use of vasoactive drugs and albumin should be tailored to the specific needs of the patient, with careful monitoring of volume status and renal function 1.

From the Research

Definition and Diagnosis of Hepatorenal Syndrome

  • Hepatorenal syndrome (HRS) is a functional form of acute kidney injury (AKI) that occurs in patients with decompensated cirrhosis 4.
  • The diagnosis of HRS is one of exclusion, and it is associated with a poor prognosis if left untreated 5.

Prerenal AKI and Hepatorenal Syndrome

  • Prerenal azotemia is a common cause of AKI in patients with cirrhosis, and it can be managed with albumin-based volume resuscitation 6.
  • However, the presence of prerenal AKI does not necessarily rule out hepatorenal syndrome, as patients with cirrhosis can have multiple etiologies of AKI simultaneously 6, 7.
  • Novel biomarkers, such as urinary neutrophil gelatinase-associated lipocalin and interleukin-18, may be able to distinguish hepatorenal syndrome from prerenal azotemia and acute tubular necrosis 7.

Treatment of Hepatorenal Syndrome

  • The definitive treatment of HRS is liver transplantation, but when this is not possible, HRS can be treated with a combination of vasoconstrictor agents and intravenous albumin 4.
  • Terlipressin, a recently approved vasoconstrictor, is likely to become the first-line standard of care for HRS, although other vasoconstrictors, such as midodrine and octreotide, may still be considered 5, 4.
  • The treatment of HRS should be tailored to the individual patient, taking into account the underlying etiology of AKI and the presence of any comorbidities 6, 8.

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This information is intended for healthcare professionals. Any medical decision-making should rely on clinical judgment and independently verified information. The content provided herein does not replace professional discretion and should be considered supplementary to established clinical guidelines. Healthcare providers should verify all information against primary literature and current practice standards before application in patient care. Dr.Oracle assumes no liability for clinical decisions based on this content.