Serum sodium < 135 mmol/L is called hyponatremia. Serum sodium only reflects a decrease in the concentration of sodium in the plasma, and does not necessarily indicate a loss of total sodium in the body; overall sodium may be normal or even slightly increased. It is more common clinically, especially in the elderly. The main symptoms are weakness, nausea and vomiting, headache and drowsiness, painful muscle spasms, neuropsychiatric symptoms and reversible ataxia. The current definition of hyponatremia in cirrhosis is a blood sodium <130 mmol/L, and its incidence is 21.6% . If defined by the lower limit of the normal reference range of blood sodium <135 mmol/L, its incidence is 49.4% [16]. Hyponatremia in cirrhosis is a more severe metabolic abnormality. There are 2 types of hyponatremia in cirrhosis: one is hypovolemic hyponatremia, which is often due to gastrointestinal loss or excessive diuresis causing water and sodium to be excreted from the kidneys, resulting in a decrease in extracellular fluid, manifesting as a decrease in blood volume with hyponatremia, without swelling, ascites, dehydrated appearance and pre-renal renal failure. The other is dilutional hyponatremia, also known as high-volume hyponatremia, which is due to impaired renal drainage, resulting in disproportionate water retention and sodium retention, and dilutional hyponatremia has more serious consequences for patients with cirrhosis. Recent studies on the mechanisms regulating water excretion in cirrhosis have shown that vasopressin (VP) is the main factor contributing to water retention. Therefore, the class of vasopressin receptor antagonists (VRAs), also known as ADH receptor antagonists, has gained attention. These drugs selectively inhibit V2 receptors located in the VP of the collecting duct principal cells and directly counteract the effects of antidiuretic hormone [16-17]. In healthy subjects, VRAs are significantly dose-dependent, resulting in an increase in urine volume accompanied by a decrease in urine osmolality. In contrast to conventional diuretics, the application of VRAs does not increase urinary sodium excretion in healthy subjects. Some studies have observed whether the use of VRAs, such as rivaraptan (1ixivaptan), tolvaptan (tolvaptan), and satavaptan (satavaptan), is effective in improving blood sodium levels in patients with hyponatremia [18-20]. The results of these studies consistently showed that short-term application of VRAs significantly improved hyponatremia. Tolvaptan for the treatment of hyponatremic patients with cirrhotic ascites has been approved by the FDA in the United States and is in phase II clinical trials in China, with preliminary results worthy of confirmation. Hyponatremia has received increasing attention from clinicians, and is closely related to the occurrence, development and prognosis of cirrhosis, and the treatment of hyponatremia is an important part of the comprehensive treatment of cirrhosis.