We thank Karaahmet et al. for their comments about our meta-analysis on vaptans in cirrhosis.[1, 2] The underlying pathogenesis of ascites and hyponatraemia is closely linked to the haemodynamic changes that occur in chronic liver failure with portal hypertension. Sodium and water restriction has been recommended as a treatment option in patients with ascites. Such regimens are difficult for the patients. Treatment with vaptans will not affect the underlying pathophysiology, but may decrease the effective arterial intravascular volume.
On the basis of the theoretical consequences of lowering the intravascular volume, we assessed changes in blood pressure and vasoactive hormones after treatment with vaptans. Vaptans did not affect systolic or diastolic blood pressure or heart rate. Our analyses found no differences in aldosterone levels, but renin levels increased, which may reflect changes in the vascular volume. Vasopressin increased during treatment with vaptans. An increase that was not sufficient to induce a V1-receptor response, as blood pressure remains unaltered. Still, an increased drive on the V2 receptors (leading to rebound water retention) could occur after discontinuation of vaptans. We did not have data that could assess a potential rebound effects.
The potential role of vaptans is not settled. It has been speculated that an increase in serum sodium may reduce the risk of hepatic encephalopathy and improve quality of life. As hyponatraemia is associated with poor outcomes after liver transplantation, vaptans may also have a role in patients who await liver transplantation. Unfortunately, we were not able to identify an effect of vaptans on these outcome measures. Our data supports the safety of vaptans and suggest that potential beneficial effects in specific subpopulations should be investigated.