Semin intervent Radiol 2015; 32(04): 445-454
DOI: 10.1055/s-0035-1564794
Clinical Corner
Thieme Medical Publishers 333 Seventh Avenue, New York, NY 10001, USA.

Hepatorenal Syndrome: A Review of Pathophysiology and Current Treatment Options

Brian Erly
1  Case Western Reserve University School of Medicine, Cleveland, Ohio
,
William D. Carey
2  Department of Gastroenterology, Cleveland Clinic, Cleveland, Ohio
,
Baljendra Kapoor
3  Section of Interventional Radiology, Imaging Institute, Cleveland Clinic, Cleveland, Ohio
,
J. Mark McKinney
4  Department of Radiology, Mayo Clinic, Jacksonville, Florida
,
Mathew Tam
5  Department of Radiology, Southend University Hospital, Essex, United Kingdom
,
Weiping Wang
4  Department of Radiology, Mayo Clinic, Jacksonville, Florida
› Author Affiliations
Further Information

Publication History

Publication Date:
10 November 2015 (online)

Cirrhosis is a result of advanced liver disease and is characterized by fibrosis of liver tissue and conversion of normal architecture into regenerative nodules,[1] [2] leading to a loss of liver function. According to the Centers for Disease Control, cirrhotic liver disease is responsible for 15,000 deaths per year in the United States.[3] [4] Portal hypertension (defined as elevation of hepatic venous pressure gradient ≥ 5 mm Hg) is a hallmark of cirrhosis, which is the result of a complicated process of inflammation, necrosis, collagen deposition, and regenerating nodules in the liver parenchyma.[5] [6] Increased portal pressure ultimately reduces portal blood flow, leading to the release of vasodilators and blood pooling in the splanchnic circulation. This results in renal hypoperfusion, with consequent activation of the renal–angiotensin–aldosterone system and fluid retention.[7] Combined with decreased oncotic forces from hypoalbuminemia, fluid leakage from the splanchnic circulation begins to exceed the capacity of the lymphatic drainage system, and ascites, a characteristic complication of decompensated cirrhosis, develops.[5] [6] [7]

In extreme cases, the maladaptive vasodilatory response can lead to hepatorenal syndrome (HRS), a rapidly progressive form of acute renal failure that occurs in patients with cirrhosis and ascites in the absence of other causes of renal failure. It is characterized by a marked reduction in glomerular filtration rate (GFR) and renal plasma flow. The hallmark of HRS is intense renal vasoconstriction with predominant peripheral arterial vasodilation. Tubular function is preserved with the absence of proteinuria or histologic changes in the kidney. HRS exists on a spectrum with milder forms of acute kidney injury in patients with cirrhosis.[8] It has been estimated that approximately 40% of patients with cirrhosis and ascites will develop HRS within 5 years, and 50% of patients hospitalized for a complication of cirrhosis will develop renal impairment, generally within a few days of admission.[9] [10] The prognosis for HRS is poor, with a mortality rate as high as 80% within 2 weeks.[11]