AVP is considered to be released in portal hypertension via baroreceptor-mediated nonosmotic stimulation induced by a decrease in effective circulation volume, which is generated by arterial splanchnic vasodilation.1 Decreased production of solute-free water along with reduction in the delivery of sodium to the distal tubule secondary to reduction in the glomerular filtration rate as well as an increase in the sodium resorption in the proximal tubule are other factors that could be responsible. Here, AVP is linked to liver disorder.