I was thinking that since there is kidney hypo perfusion due to splanchnic vasodilation (hepatorenal syndrome), reduced filtration coupled with activation of the RAAS would lead to increased sodium concentration.. So how is there hyponatremia ?
Remember that ATII is not the only vasoconstrictor, ADH is also released in this situation due to the splanchnic dilation (there are osmoreceptors that mediate it's releases that are probably the primary factor and also volume sensors, ATII incidentally is another factor that can lead to release). Anyway the increase in ADH leads to a preferential retention of free water leading to relative hyposmolarity and hyponatremia.
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