I. Metabolic disorders in chronic kidney disease 1, protein metabolism disorders in chronic kidney disease is the most prominent manifestation of protein metabolism disorders, there are usually two major results: ① protein metabolites accumulation (i.e. azotemia): can cause symptoms in various systems. ② malnutrition: including blood albumin, pre-albumin, immunoglobulin, complement and tissue protein water in the decline, plasma and tissue levels of essential amino acids decreased, some non-essential amino acid levels increased, etc., affecting the prognosis and quality of life; obvious malnutrition can cause CRF patients with reduced quality of life, increased anemia, decreased immunity, increased opportunities for infection, multiple system dysfunction and increased mortality. The significant malnutrition may result in decreased quality of life, increased anemia, decreased immunity, increased chance of infection, multiple system dysfunction and increased mortality. 2, water, electrolytes and acid-base balance In patients with chronic kidney disease, metabolic disorders of sodium, potassium, chloride, calcium, phosphorus, magnesium and other electrolytes and metabolic acidosis are very common. The above metabolic abnormalities can cause clinical manifestations of multiple system dysfunction in C RF patients, which can be life-threatening in serious cases (such as severe sodium retention, hyperkalemia, etc.), and can also adversely affect the metabolism of other nutrients (such as protein). 3, abnormal glucose metabolism mainly manifested as low glucose tolerance, occasionally occurring hypoglycemia. Metabolic acidosis, hyper-PTHemia and uremic toxins (such as methylguanidine) can affect the regulation of blood glucose by insulin. 4. Abnormal lipid metabolism Hyperlipidemia is quite common in patients with chronic kidney disease. It is manifested as mild to moderate hypertriglyceridemia or/and mild hypercholesterolemia. Lipoprotein abnormalities are manifested by elevated plasma lipoprotein a and very low density lipoprotein levels, while high density lipoprotein levels are significantly lower, while low density lipoprotein levels are mostly normal. Second, the significance of nutritional therapy in chronic kidney disease 1. Studies have shown that a low-protein diet does not affect the survival rate and the incidence of complications. Moreover, as long as the essential amino acids or their keto acids and sufficient energy are supplemented, a good nutritional level can be maintained. 2. The use of essential amino acids (EAA) + α-keto acid therapy can help patients to reuse urea nitrogen by replenishing essential amino acids, thus promoting protein synthesis in the body and reducing the concentration of nitrogen metabolites in the blood, and partially relieving the corresponding symptoms caused by nitrogen metabolites. Nutritional therapy can also inhibit protein catabolism/ or improve protein synthesis by correcting metabolic acidosis to reduce the accumulation of some uremic toxins: by reducing endocrine disorders (hyperparathyroidism, insulin resistance, etc.). Make its corresponding complications such as renal bone disease, skin pruritus, gastrointestinal bleeding,, hypertension and other clinical manifestations reduced. 3, delay the progression of chronic kidney disease Protein diet can significantly affect the renal hemodynamics, which in turn changes glomerular filtration. A low-protein diet can reduce hyperfiltration and decrease the degree of kidney unit damage. Specific implementation of nutritional therapy: restrict protein intake: ① in the compensated phase of renal insufficiency (GFR 50-80 ml/min): a normal diet of 1 g.kg-1.d-1 (70 g) can be used; ② in the decompensated phase of renal insufficiency (GFR 20-50 ml/min) and renal failure (GFR 10 -20ml/min): low protein and low phosphorus diet with 0.5-0.6g.kg-1.d-1 protein (about 35-45g) and 5-10mg.kg-1.d-1 phosphorus, plus α-keto acid or essential amino acid preparation (0.1-0.15g.kg-1.d-1); (iii) uremic phase (GFR