Hepatorenal Syndrome

Hey Shamik,
I have a patient with alcohol-induced cirrhosis and ascites. In addition, he was found to be in acute renal failure at admission with a Cr 1.5 from baseline 0.8. My concern was his kidneys, and my question was regarding hepatorenal syndrome, the most dreaded complication of cirrhosis.

I did some research, which I thought was interesting. The mechanism of hepatorenal syndrome is multifaceted and still not fully elucidated. However, following the development of cirrhosis and portal hypertension, there is increased pressure within the splanchnic circulation, leading to increased production of nitric oxide. This causes local vasodilation of the splanchnic vasculature and pooling of blood. As such, there is reduced effective arterial blood volume, which kicks in the RAAS system. Consequently, there is renal vasoconstriction and decreased GFR.

There are two types of hepatorenal syndrome: type I is very bad with a survival of 2 weeks. With type I, there is a doubling of Cr usually above 2.5 and Cr clearance is generally less than 20. Type II, however, is more insidious; Cr is usually around 1.5 and clearance around 40. It is classically associated with ascites refractory to diuretics.

So, with my patient, I gave him a fluid challenge. This was somewhat counterintuitive because he had ascites and 2+ LE edema; he appeared outwardly volume up. However, in order to rule-out hepatorenal syndrome, the key is to rule-out renal failure of other causes, namely pre-renal. Notably, I also ordered a FEurea, which is more accurate than a FENa in the context of recent diuretic use; less than 35% is pre-renal. My patient was at 34%.

His albumin was 1.0, and he had a stable iron deficiency anemia. Instead of giving 1L NS, I gave him 1 unit of blood to both increase his circulating volume as well as his oncotic pressure. Then, I gave him a 500cc fluid bolus with IV NS. I figured that it would be useful to increase his oncotic pressure first and then give fluid as the NS would stay intravascular better--no evidence but it sounded logical.

His kidneys responded, and his Cr came down to baseline. He was pre-renal. What did I learn from this case:

1. Cirrhotics can be outwardly volume up (eg., ascites and edema) but intravascularly volume down (often from aggressive diuresis).
2. To rule-out hepatorenal syndrome, first consider the history, ie, has this patient been aggressively diuresed?
3. In the absence of history, check a FEurea and/or give a fluid bolus. I liked the idea of giving blood instead of NS in the context of anemia; kill two birds with one stone (ie, anemia and pre-renal failure). Obviously though, there are risks to giving blood products...
4. If the patient doesn't respond, further assess for hepatorenal syndrome. Apparently, dopplers of the renal arteries can assist with the diagnosis. I never got to that point, thankfully.
5. Lastly, a word about diuresis. Never forget to add a spironolactone to your lasix. Remember the RAAS pathway and the importance of inhibiting aldosterone!