Hepatorenal syndrome (HRS) is a potentially reversible, functional renal failure resulting from circulatory dysfunction. It is considered the most severe and frequently final complication of end-stage liver disease (ESLD) and usually develops in the setting of cirrhosis and ascites.¹ In HRS, renal dysfunction occurs in the absence of intrinsic renal disease, with the pathophysiological hallmarks of intense renal cortical vasoconstriction, severe sodium retention, and oliguria.^2,3 Without intervention to restore normal renal function, the natural course of renal failure in HRS is usually progressive to an inevitable fatal outcome.⁴ Complete reversal of renal failure with arteriographic normalization of renal vascular abnormalities has been observed with a variety of therapeutic maneuvers for HRS, including liver transplantation (to treat its cause)3 and a combination of vasoconstrictor (vasopressin analogs) and albumin administration.⁵

Pathogenic Concepts
Hepatorenal syndrome occurs most commonly in the setting of cirrhosis, portal hypertension,² and ascites.⁶ The increased resistance to portal flow as a consequence of liver disease triggers changes in the intestinal microcirculation that result in vasodilatation. There is a compensatory increase in plasma volume and cardiac output in the presence of reduced peripheral vascular resistance, giving rise to the characteristic hyperdynamic circulation associated with cirrhosis.⁴ Increasing splanchnic arteriolar vasodilatation secondary to worsening portal hypertension results in progressively severe arterial hypotension and a marked decline in effective arterial blood volume. The resultant underfilling ensures continued activation of the renin–angiotensin–aldosterone system and sympathetic nervous system and, ultimately, increased antidiuretic hormone secretion. This produces renal vasoconstriction, a prominent decrease in renal perfusion and glomerular filtration rate, and progressive azotemia (see Figure 1).^4,7,8

To register to view full article click here