Homocysteine (HCY), also known as homocysteine, is a sulfur-containing amino acid formed after the demethylation of methionine and is an intermediate product of the methionine cycle. HCY is derived from dietary intake of methionine and is a product of the hydrolysis reaction of S-adenosine HCY in the methionine cycle and, at the same time, is a substrate for the synthesis of cystathione by cystathione beta synthase. The range of plasma HCY in normal subjects varies somewhat due to different measurement methods. The generally accepted standard is 5-15.9 μmol/L in normal subjects, and the criteria for diagnosing mild, moderate, and severe hyperplasma homocysteinemia are 16-30 μmol/L, 30-100 μmol/L, and greater than 100 μmol/L, respectively. Approximately 70% of HCY in fresh plasma exists in the form of disulfide bonds bound to albumin. Only about 20% is in the free state. Storage of plasma causes redistribution of these two parts, with an increase in the bound part and a decrease in the free part, so it is better to measure total HCY when measuring. Vascular disease In addition to abnormalities such as mental retardation and skeletal malformations, patients with hereditary homocystinuria often have more extensive and significant vascular lesions in large and small arteries and veins, and elevated plasma HCY concentrations are the only metabolic disorder in this hereditary disease. Chronic renal insufficiency (CRF) hyperHCYemia is seen in all stages of CRF and in patients treated with various modalities, and HCY is the most common risk factor for occlusive vascular disease in CRF patients. The mechanisms underlying the development of hyperHCYemia in CRF remain unclear. HyperHCYemia is present in patients treated with hemodialysis regardless of the dialysis modality. Hemodialysis decreases plasma HCY levels by about 30%, which may be due to the fact that most HCY is present in the plasma in the albumin-bound form. Hemodialysis only removes some of the free HCY; therefore, although dialysis can reduce plasma HCY levels to some extent, it is difficult to restore them to normal. Vitamins B6, B12 and folic acid, which are involved in HCY metabolism, can cause varying degrees of decrease in their levels. The use of these drugs without significant side effects to lower the plasma HCY levels of patients is beneficial in reducing the incidence of cardiovascular disease.