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SMJ // Article

Expired CME Article

Hepatorenal Syndrome

Authors: Deepak Venkat, MD, K. K. Venkat, MD

Abstract

Acute kidney injury (AKI) secondary to hepatorenal syndrome (HRS) is an ominous complication of end-stage liver disease (ESLD). In HRS, splanchnic and peripheral vasodilatation with reduction in effective arterial volume causes activation of mechanisms leading to intense renal vasoconstriction and functional AKI. HRS is a diagnosis of exclusion and all other causes of AKI (especially prerenal azotemia) have to be considered and excluded. Spontaneous bacterial peritonitis (SBP) frequently precipitates HRS and should be ruled out in all ESLD patients presenting with AKI. Prompt therapy of SBP with intravenous antibiotics and albumin lessens the risk of developing HRS. Combined use of intravenous albumin, splanchnic and/or peripheral vasoconstrictors, and renal replacement therapy (RRT) are only bridges to early liver transplantation (or combined liver-kidney transplantation in selected patients). Transplantation is the only definitive way of improving the long-term prognosis. Close collaboration between hospitalists/internists managing HRS patients and hepatology and nephrology consultants is critically important.


Key Points


* Hepatorenal syndrome (HRS) is a unique form of acute kidney injury (AKI), which develops in patients with advanced chronic (cirrhosis) or acute fulminant liver disease.


* It is caused by severe renal vasoconstriction without structural changes in the kidneys in the setting of splanchnic and peripheral vasodilatation resulting in a pooling of blood in the vasodilated areas with consequent decreased effective arterial volume and renal hypoperfusion.


* HRS is a diagnosis of exclusion: all other causes of AKI not unique to patients with advanced liver disease must be ruled out.


* Management requires combined use of splanchnic and peripheral vasoconstrictors and volume expansion with intravenous albumin, percutaneous transjugular intrahepatic portosystemic shunting (in selected patients), treatment of spontaneous bacterial peritonitis (a common precipitant of HRS), if present, and renal replacement therapy (intermittent or continuous), if indicated.


* All of the above measures are only bridges to early liver transplantation, which is the only effective way to improve the long-term prognosis of these patients.

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