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Hepatorenal syndrome (HRS) refers to a unique type of kidney injury that occurs in patients with cirrhosis and ascites. The pathophysiology is not well understood but is likely due to splanchnic vasodilation in the setting of portal hypertension. HRS may develop rapidly in the case of HRS acute kidney injury (HRS-AKI) or gradually in the case of HRS non-acute kidney injury (HRS-NAKI). It is a diagnosis of exclusion and requires the elimination of other potential etiologies, including hypovolemia. A liver transplant is the only curative treatment, but it may be mitigated pharmacologically with vasoconstrictors and albumin.
A unique phenotype of kidney injury in patients with cirrhosis and ascites in the absence of hypovolemia or other kidney pathology. It is further split into: 
- HRS-acute kidney injury (HRS-AKI): acute kidney injury in patients with cirrhosis (see “Diagnostic criteria for HRS-NAKI” below); formerly known as type 1 HRS
- HRS-non-acute kidney injury (HRS-NAKI): functional kidney injury in patients with cirrhosis not meeting the criteria for HRS-AKI; formerly known as type 2 HRS
- Complication of liver failure, especially cirrhosis
- The exact pathomechanisms are not completely understood: Cirrhosis/portal hypertension → ↑ splanchnic vasodilators (e.g., nitric oxide) → ↓ arterial blood flow → activation of RAAS → renal vasoconstriction → ↓ GFR 
- Risk factors/triggers may include:
Hepatorenal syndrome (HRS) is a diagnosis of exclusion. It is diagnosed based on the presence of renal impairment in patients with cirrhosis after other potential causes of renal impairment have been ruled out. 
- Initial evaluation
Diagnostic criteria for HRS-AKI 
- Presence of cirrhosis with ascites
Diagnosis of AKI according to the following criteria: 
- An increase in serum creatinine of ≥ 0.3 mg/dL within 48 hours or to ≥ 1.5 times baseline within a 7-day period
- And/or urine output ≤ 0.5 mL/kg for ≥ 6 hours
- No improvement after two consecutive days of albumin infusions and diuretic withdrawal
- Absence of shock
- No current or recent nephrotoxic agents
- Absence of signs of structural kidney disease
Treatment for HRS-AKI should always be combined with adequate management for cirrhosis, and a multidisciplinary team should be involved as soon as possible. Data on effective treatments for HRS-NAKI is lacking. 
Pharmacotherapy for HRS-AKI 
- Preferred: vasoconstrictor (either terlipressin OR norepinephrine) PLUS albumin
- Alternative: combination of midodrine; PLUS octreotide
Surgical or interventional options 
- Renal replacement therapy (mainly hemodialysis) 
- A liver transplant is the only curative option.
- TIPS placement is not routinely recommended. 
- General measures: prevention of GI bleeding and bacterial infections, avoidance of large-volume paracentesis without concurrent albumin administration
- Specific measures: IV albumin with antibiotics reduces the risk of patients with spontaneous bacterial peritonitis developing HRS-AKI.
Vasoconstrictor therapy is challenging and has potentially severe adverse effects (e.g., ischemia); involve specialists early.