Which one of these mechanisms is responsible for sodium retention in cirrhosis and hepatorenal syndrome?
Decreased " effective " plasma volume 64%
Increased vascular capacitance 0%
Cirrhosis alone 0%
Abnormal hepatic vascular function and hepatic vascular sensor 14%
jury still out 21%
Tough question. There might be no right or wrong answer but I think the best answer is the jury is still out.
I defer you to the above linked recent Kidney International article that reviews the latest research in hepatorenal syndrome.
some points to make:
1. The "effective" plasma volume concept has been the one that most people think of as the cause of this syndrome. The questions really are to ask where is this effective plasma volume decreased. In recent studies, patients with cirrhosis, plasma volume remained unchanged after ascites removal and there was some thought that the renal salt and water retention preceded ascites and edema. Another study, showed that measures total plasma volume had really increased in most subjects and even in the splanchnic and non splanchnic beds. This study showed that it was the ascites and edema in cirrhosis resulted from a positive sodium and water balance.
2. The concept of increased vascular capacitance is there. This in contrast to the above "overfilling" , is the under filling hypothesis. Here the primary event in edema formation is really systemic vasodilation caused by cirrhosis itself perhaps via nitric oxide. This leads to the edema due to underfilling and a results " low plasma volume" and salt retention. This has been a newer hypothesis.
3,4 There is data now coming out that the liver itself has intra hepatic vascular sensors that sense and regulate renal function, thirst and salt appetite. So basically, there are baroreceptors capable of regulating renal sympathetic activity. Its possible that this baroreflex remains active during cirrhosis and continues to cause this increased renal sympathetic activity as a result.
So i guess after all this, probably, we still don't know!
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