From the Guidelines
Hepatorenal Syndrome (HRS) is diagnosed based on the presence of cirrhosis with ascites, acute kidney injury (AKI), and absence of other potential causes of kidney disease.
Diagnostic Criteria
The diagnostic criteria for HRS include:
- Cirrhosis with ascites
- Diagnosis of AKI according to the International Club of Ascites (ICA-AKI) criteria, which includes an increase in serum creatinine of ≥0.3 mg/dL within 48 hours or ≥50% from baseline 1
- No response after 2 consecutive days of diuretic withdrawal and plasma volume expansion with albumin 1 g/kg body weight 1
- Absence of shock
- No current or recent use of nephrotoxic drugs
- No macroscopic signs of structural kidney injury, defined as:
- Absence of proteinuria (>500 mg/day)
- Absence of microhaematuria (>50 RBCs per high power field)
- Normal findings on renal ultrasonography 1
Classification of HRS
HRS is classified into two types:
- HRS-AKI (Acute Kidney Injury): characterized by a rapid and progressive impairment in renal function, with an increase in serum creatinine of ≥0.3 mg/dL within 48 hours or ≥50% from baseline 1
- HRS-NAKI (Non-Acute Kidney Injury): characterized by a stable or less progressive impairment in renal function 1 The diagnosis of HRS requires a comprehensive evaluation of the patient's clinical presentation, laboratory results, and imaging studies, as outlined in the guidelines from the International Club of Ascites 1 and the American Association for the Study of Liver Diseases 1.
From the Research
Diagnostic Criteria for Hepatorenal Syndrome (HRS)
The diagnostic criteria for HRS have undergone revisions over the years, with recent updates aiming to improve accuracy and reflect the complex pathophysiology of the condition 2, 3. The key characteristics of HRS include:
- Severe impairment of kidney function due to increased splanchnic blood flow, activation of vasoconstriction factors, and severe vasoconstriction of the renal arteries in the absence of kidney histologic abnormalities 2
- Systemic inflammation, oxidative stress, and bile salt-related tubular damage may contribute to the development of HRS 3
- Lack of specific diagnostic biomarkers to distinguish structural from functional acute kidney injury (AKI) 2, 4
Classification of HRS
HRS has been classified into two types:
- HRS Type 1 (HRS-AKI): characterized by a rapid deterioration of renal function, often due to a precipitating event 3, 4
- HRS Type 2 (HRS-2): characterized by a moderate and stable or slowly progressive renal dysfunction, often without an obvious precipitant 3
Diagnostic Challenges
The diagnosis of HRS remains a challenge due to the lack of specific diagnostic biomarkers and the need for differential diagnosis from other forms of AKI, particularly acute tubular necrosis 2, 4. Recent studies have explored the use of urinary biomarkers, such as neutrophil gelatinase-associated lipocalin, to objectively phenotype etiologies of AKI in patients with cirrhosis 4.
Clinical Features and Precipitating Factors
Clinical features of HRS include hepatic encephalopathy, jaundice, and refractory ascites 5. Precipitating factors for HRS include infection, GI bleeding, and over paracentesis 5. Alcohol abuse is a common predisposing factor for the development of HRS 5.
Treatment and Outcome
Treatment options for HRS include vasoconstrictor drugs, such as terlipressin, and plasma volume expansion by intravenous albumin infusion 2, 6. The response to treatment is variable, with age being an independent predictor of response 6. Three-month survival of patients with HRS Type 1 is approximately 20% 6, with mortality strongly predicted by simple baseline variables, such as age, bilirubin, and creatinine increase after diagnostic volume expansion 6.