Syndrome of abnormal secretion of antidiuretic hormone (SIADH) is a group of syndromes with abnormally increased secretion of endogenous antidiuretic hormone (ADH, i.e., arginine pressor AVP) due to multiple causes and inappropriately high plasma antidiuretic hormone concentrations relative to body fluid osmolality, resulting in clinical manifestations related to water retention, increased urinary sodium excretion, and dilutional hyponatremia. According to the characteristics of ADH secretion, Robertson et al. divided SIADH into 4 types, and the following explains how to initially examine each type of SIADH. Type I Also known as type A, accounting for about 37% of the cases, the secretion of ADH is irregular and not regulated by blood osmolarity, showing autonomic secretion. SIADH caused by respiratory system diseases mostly belongs to this type. Type II, also known as type B, accounts for about 33% of cases, and the secretion of ADH is regulated by blood osmolality, but the point of regulation is shifted downward. It is believed that this type of SIADH is the reset osmotic syndrome. It has been suggested that osmotic domain reregulation syndrome is caused by inappropriate accumulation of osmotic substances (both electrolytes and nonelectrolytes) in osmolarity receptor cells, causing the osmolarity receptors to mistake normal for hyperosmolarity and triggering the release of ADH. For this reason, this syndrome was also formerly known as sick cell syndrome. SIADH caused by bronchopulmonary carcinoma and tuberculous meningitis is often of this type. Type III, also known as type C, accounts for about 16% of cases. ADH secretion is regulated by blood osmolality, but the regulation is partially impaired. When the plasma osmolality is lowered below the regulation point, some people call this ADH secretion as vasopressin leak. Most of the SIADH caused by CNS diseases belongs to this type. Type IV, also known as type D, accounts for about 14%. The body’s ADH secretion regulation mechanism is intact and the plasma ADH level is normal, but the sensitivity of the kidney to ADH is increased. It is also believed that ADH-like substances are present in this type of patient, and it is the ADH-like substances rather than ADH itself that cause the clinical manifestations. Strictly speaking, the term SIADH does not apply to this type because there is no inappropriate secretion of ADH, but it is still customary to classify this type as SIADH.