Hyponatremia in cirrhosis. Pathophysiology, prevalence, prognostic value, treatment.

Hypervolemic hyponatremia is common in patients with decompensated cirrhosis, resulting from solute-free water retention caused by the stimulation of V2 receptors of the distal nephron by relatively high circulating levels of arginine vasopressin (AVP, a nonapeptide). A nonosmotic secretion of AVP by the hypothalamo-neurohypophysial system is responsible for high plasma AVP concentrations. This hypersecretion of AVP is triggered by a decrease in effective arterial blood volume and arterial pressure caused by splanchnic/systemic vasodilation. Hyponatremia is an independent predictor of mortality in patients with cirrhosis; however, it is still unknown if hyponatremia by itself plays a role or if it is a simple marker of the severity of liver disease. Pharmacological treatments of hypervolemic hyponatremia using drugs that antagonize the binding of AVP to V2 receptors are under evaluation in patients with cirrhosis.