When cirrhosis enters the decompensated stage, hypoalbuminemia will appear, which is caused by malnutrition, insufficient synthesis and excessive loss. When the plasma albumin decreases, the effective osmotic pressure decreases, causing excessive water retention in the tissues, resulting in swelling, and in severe cases of swelling, pleural fluid and ascites may appear. Gastrointestinal mucosa atrophy, reduced gastric acid secretion, reduced digestive enzymes, poor appetite, fatigue, weakness are also common symptoms, the patient does not like to move, physical strength decreases, the response becomes slower, memory loss. There is mostly mild to moderate anemia, frequent dizziness, and there may be postural hypotension and bradycardia. These are the serious consequences written in the book. Case sharing: The patient, 40 years old, had 10 years of post-hepatitis B cirrhosis loss of compensation with primary hepatocellular carcinoma for 3 years. Almost all complications of cirrhosis in these 10 years had appeared in him, including ascites, hepatic encephalopathy, gastrointestinal bleeding, spontaneous peritonitis and primary hepatocellular carcinoma. The most recurrent was ascites, but usually small amounts, and moderate amounts were eliminated with medical treatment. This patient’s hypoproteinemia can be seen to hover between 10g-20g/l for a long time, even in single digits, and can only be maintained for a short time after massive infusions. However, this patient is currently living well and does not have many of the discomforts mentioned above. In particular, there is no appearance of massive ascites or even intractable ascites. How much of a role does hypoproteinemia play in the formation of ascites? The mechanism of ascites in cirrhosis is not completely clear, and there are three major theories about the mechanism of ascites formation in cirrhosis, namely the “underfilling and perfusion theory”, the “pancytopenia theory” and the “visceral vasodilatation theory “. Even the “visceral vasodilatation theory”, which is agreed by most researchers, cannot fully explain the mechanism of ascites. This leads to a decrease in effective blood volume, lower cardiac output, activation of the renin-angiotensin-aldosterone system, and stimulation of sympathetic nervous system excitation and antidiuretic hormone release, causing sodium and water retention, which leads to ascites production under the synergistic effect of portal hypertension. Recently, the “three-stage theory” has been proposed for the occurrence mechanism of ascites in cirrhosis, that is, ascites formation is divided into three stages: early, middle and late. Early ascites refers to the period of hypoalbuminemia, and its formation mechanism is the combined effect of hypoalbuminemia and portal hypertension, which disrupts the Starling balance of visceral microcirculation, and the production of lymphatic fluid is greater than absorption, resulting in ascites, which is consistent with the Backward theory. Mid-stage ascites refers to the period of neuroendocrine disorder, and the mechanism of its occurrence is that on the basis of early ascites formation, the reduction of effective blood volume due to ascites formation or the inappropriate use of diuretics aggravates the reduction of blood volume, which activates sympathetic nerves, volume receptors of heart and lungs and renin secretion of glomerulus, and the release of hormones such as antidiuretic hormone and aldosterone leads to water and sodium retention and renal artery constriction, thus increasing blood volume in In concert with portal hypertension, visceral vasodilatation, increased hydrostatic pressure, and increased NO synthesis aggravate ascites production. The difference between intermediate ascites formation and the “pancytopenia theory” is that we believe that sodium and water retention is the result of neuroendocrine disorders secondary to decreased blood volume in ascites formation, and that sodium and water retention exacerbates the formation of ascites, rather than the traditional belief that sodium and water retention triggers ascites production. Late ascites refers to the refractory ascites stage, the main characteristics of patients in this stage are refractory ascites, severe hyponatremia, cardiac hypoperfusion and hepatorenal syndrome, the mechanism of its occurrence lies in further sodium-water retention on the basis of mid-stage ascites, and more water retention than sodium retention, severe hyponatremia causing extreme activation of the renin-angiotensin-aldosterone system and severe constriction of the renal arteries, leading to the development of hepatorenal syndrome and Renal tubular necrosis occurs in the kidney under long-term ischemia, leading to the transformation of the kidney from functional damage to renal parenchymal damage. Even with the use of terlipressin plus albumin expansion in this stage, the treatment did not help to reduce ascites and hepatorenal syndrome. In summary, we believe that: hypoalbuminemia is a key factor in the formation of ascites in patients with cirrhosis in early stages, and timely administration of albumin infusion to cirrhotic patients with hypoalbuminemia is an important measure to prevent and treat ascites in early stages of cirrhosis. However, by the middle and late stages, the treatment of ascites does not need to rely excessively on albumin infusion. The clearance of ascites can be achieved in this patient with just very little albumin therapy (10g/month).