Today’s lecture focused on the diagnosis and treatment of hepatorenal syndrome. With respect to diagnosis, there has been a shift over the years away from incorporating urinary sodium as a criterion (UNa < 10); it is no longer used, though some argue it is still a valuable indicator. For HRS-1, there should be a doubling of serum creatinine over a two week period (to a level > 2.5) in the presence of cirrhosis and absence of intrinsic renal disease. Lastly, a two day volume challenge/failure with 100 mg of albumin per day is required. This is in contrast to previous criteria that did not specify albumin over other volume expanders like saline.
With respect to treatment, not a lot has changed since the International Ascites Club met in 2003. It is clear that albumin should be used as an adjunct to whatever vasoactive compounds are started. The speaker was not enthusiastic about the efficacy of octreotide and midodrine, though some in the audience disagreed. An Italian center published a head to head trial of octreotide/midodrine vs. terlipressin and found the later to be superior. It is important to recognize that these vasoactive products can reverse the syndrome; there is conflicting evidence whether they prolong transplant-free survival. Liver transplantation is still the best treatment.
Interestingly, there were two comments about cirrhotic cardiomyopathy in this talk. First was how the cirrhotic heart plays a distinct role in the development of hepatorenal syndrome, with poor forward flow (in cases of systolic dysfunction) contributing to decreased renal inflow. Second was the notion of the cirrhotic heart being partly responsible for those who do vs do not respond to treatment with albumin and vasoactive compounds.
Lastly, and not least importantly, is that any patient with new HRS-1 should be referred to the on site study coordinators for prospective enrollment into a clinical trial of terlipressin. After all, only 10% of referred patients eventually get enrolled.