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How is hepatorenal syndrome diagnosed?
The diagnostic criteria for hepatorenal syndrome were updated by the IAC in 2015. This followed the adaptation of a set of uniform nomenclature and diagnostic criteria for Acute Kidney Injury.
The below table outlines the diagnosis, staging, and definitions of progression/regression of Acute Kidney Injury as proposed by the IAC.
Diagnosis, Staging and Assessing Response to Treatment of Acute Kidney Injury in Patients With Cirrhosis According to International Ascites Club
| PARAMETER | DEFINITION |
|---|---|
| Baseline SCr | Stable SCr in ≤ 3 months If not available, a stable SCr closest to the current one If no previous SCr at all, use admission SCr |
| Definition of AKI | ↑ in SCr ≥ 0.3 mg/dL (26.4 µmol/L) ≤ 48 h, or ↑ 50% from baseline |
| Staging | Stage 1: ↑ SCr ≥ 0.3 mg/dL (26.4 µmol/L) or ↑ SCr ≥ 1.5–2.0 X from baseline Stage 2: ↑ SCr > 2.0–3.0 X from baseline Stage 3: ↑ SCr > 3.0 X from baseline, or SCr ≥ 4.0 mg/dL (352 µmol/L) with an acute ↑ of ≥ 0.3 mg/dL (26.4 µmol/L), or initiation of renal replacement therapy |
| Progression | Progression of AKI to a higher stage, or need for renal replacement therapy |
| Regression | Regression of AKI to lower stage |
| Response to treatment | None: No regression of AKI Partial: Regression of AKI stage with a ↓ in SCr to a value ≥ 0.3 mg/ dL (26.4 µmol/L) above baseline Complete: ↓ SCr < 0.3 mg/dL (26.4 µmol/L) from baseline |
AKI , Acute kidney injury; IAC , International Ascites Club; SCr , serum creatinine.
From Angeli, P., Gines, P., Wong, F., et al. (2015). Diagnosis and management of acute kidney injury in patients with cirrhosis: revised consensus recommendations of the International Club of Ascites. Gut, 64(4):531–537.
It is possible that patients who fulfill these criteria may still have structural damage, such as acute tubular necrosis (ATN). Urine biomarkers will become an important element in making a more accurate differential diagnosis between HRS and ATN.
Urinary electrolyte criteria are not required for the diagnosis of AKI-HRS, and the presence of infection does not preclude its diagnosis.
Using these criteria, Acute Kidney Injury is defined as an increase in serum creatinine by 0.3 mg/dL in less than 48 hours, or a 50% increase in serum creatinine presumed to have occurred in the past 7 days from baseline. Type 1 HRS or AKI-HRS is a special type of AKI that is not responsive to volume replacement.
The new diagnostic criteria of AKI-HRS as set out in 2015 modified the previous criteria set by the IAC in 2007. There has to be at least a doubling of serum creatinine without setting an absolute creatinine level (i.e., 2.5 mg/dL) for the diagnosis. The current proposed diagnostic criteria for AKI-HRS are:
• Cirrhosis and ascites
• Diagnosis of AKI according to the IAC-AKI criteria
• No reduction in serum creatinine after at least 48 hours of diuretic withdrawal and volume expansion with albumin. The recommended dose of albumin is 1 g/kg body weight/day up to a maximum of 100 g/day.
• Absence of shock
• No current or recent treatment with nephrotoxic drugs
• No evidence of structural kidney injury defined as:
• Absence of proteinuria (>500 mg/day)
• Absence of hematuria (>50 red blood cells/high power field)
• Normal kidney ultrasonography
