Chapter outlines
Definitions and classification |
Pathogenesis |
Diagnosis |
Prevention |
Management |
General measures |
Pharmacological therapy |
- Albumin |
- Vasoconstrictors |
Non-pharmacological therapy |
- Renal replacement therapy |
- Transjugular intrahepatic portosystemic shunt |
- Liver transplantation |
- Simultaneous liver-kidney transplantation |
Kidney failure is the most frequent organ failure in patients with acute or chronic liver disease, with a frequency of 20–50% in hospitalized cirrhotic patients [1–3].
Hepatorenal syndrome (HRS) is a life-threatening complication and one of many causes of acute kidney injury in patients with acute or chronic liver disease. HRS frequently occurs in hospitalized patients and is associated with a high mortality rate (about 32 to 37%) [4–6], readmission rate (about 23%) [5], hospital and health care costs [6, 7], and longer stay in hospital [4].
The most common precipitating factors of HRS are gastrointestinal bleeding, large volume paracentesis, diuretics, non-steroidal anti-inflammatory drugs (NSAIDs), spontaneous bacterial peritonitis, and other infections [5, 8].
DEFINITIONS AND TYPES OF HEPATORENAL SYNDROME
Hepatorenal syndrome is a specific cause of acute kidney injury (AKI) frequently encountered in advanced cirrhosis characterized by rapidly progressive renal failure, which occurs without apparent pathologic abnormalities in the kidneys [9].
Hepatorenal syndrome is traditionally classified into Type 1 and Type 2 HRS based on the severity of diseases reflected by the rapidity of decline in kidney function [10]. Type 1 (HRS-1) is a serious form of AKI that occurs in advanced cirrhosis with ascites.
Type 1 HRS is characterized by a rapid and progressive reduction in renal function (a 2-fold increase of serum creatinine to at least 2.5 mg/dL or a decrease of creatinine clearance by 50% to less than 20 mL/min within 2 weeks) [11], and has a poor prognosis (median survival only 8 to 12 weeks) [12]. Type 2 HRS is a less severe form of kidney function impairment that is slowly progressive and clinically characterized by ascites resistant to diuretics [11] and has a median survival of about 6 months [12].
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