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Contemporary Reviews in Critical Care Medicine |

Hepatorenal DisordersHepatorenal Disorders

Ali Al-Khafaji, MD, MPH; Mitra K. Nadim, MD; John A. Kellum, MD
Author and Funding Information

From the Center for Critical Care Nephrology (Drs Al-Khafaji and Kellum), and The CRISMA (Clinical Research, Investigation and Systems Modeling of Acute Illness) Center (Drs Al-Khafaji and Kellum), Department of Critical Care Medicine, University of Pittsburgh School of Medicine, Pittsburgh, PA; and the Department of Medicine (Dr Nadim), University of Southern California, Los Angeles, CA.

CORRESPONDENCE TO: John A. Kellum, MD, Center for Critical Care Nephrology, Department of Critical Care Medicine, University of Pittsburgh, 604 Scaife Hall, 3550 Terrace St, Pittsburgh, PA 15261; e-mail: Kellumja@upmc.edu


Reproduction of this article is prohibited without written permission from the American College of Chest Physicians. See online for more details.


Chest. 2015;148(2):550-558. doi:10.1378/chest.14-1925
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Renal dysfunction is common in patients with end-stage liver disease (ESLD); it takes on many forms from acute to chronic renal injury and may involve a variety of mechanisms. Hepatorenal syndrome (HRS) is a specific type of hepatorenal disorder (HRD) with a unique pathophysiology. HRS is characterized by splanchnic arterial vasodilatation and decreased effective intravascular volume that leads to renal vasoconstriction and decreased renal blood flow. The incidence of HRS in relation to other forms of HRD is unknown; however, it is estimated that 35% to 40% patients with ESLD and ascites eventually develop the condition. Two subtypes of HRS have been described. Type 1 HRS is rapidly progressive, whereas the renal function in type 2 HRS deteriorates slowly over weeks or months. Type 1 HRS may be precipitated by sepsis or acute alcoholic hepatitis and occasionally develops in patients who already have type 2 HRS. The diagnosis of HRS is based on the exclusion of other causes of renal dysfunction because no specific test is available. The definitive treatment of HRS is liver transplant. As a bridge to liver transplant, medical management with volume expansion and the use of vasoconstrictors is often implemented. A transjugular intrahepatic portosystemic shunt has been attempted in treating HRS, although there is little evidence of its efficacy compared with standard therapy. Renal replacement therapy is often used if the patient is a liver transplant candidate. Artificial liver assist devices are in the research phase.

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