Diabetes insipidus (DI) is a clinical disorder characterized by an excessive hypotonic and diluted urine output. There are four main mechanisms involved in the pathophysiology of DI: (1) central DI (CDI), when the main alteration occurs in the hypothalamus or posterior pituitary and an insufficient amount of the antidiuretic hormone (ADH or AVP) is synthesized or released; (2) nephrogenic DI (NDI), when the kidney does not respond correctly to AVP; (3) transient DI of pregnancy, where an altered AVP metabolism occurs, presumably during a limited period of time; and (4) primary polydipsia, where the initial pathogenic mechanism is related to the intake of fluid, and not as much in its excretion. Consideration of the basic physiopathologic mechanisms involved in AVP regulation enables subsequent understanding of the potential diagnostic and treatment alternative tools for a patient with DI. In this chapter, we will thoroughly revise the different clinical settings of DI, and we will discuss the algorithms that need to be followed for a correct approach and management of patients with this syndrome.
Diabetes insipidus Central diabetes insipidus Nephrogenic diabetes insipidus Desmopressin, pituitary surgery Aquaporin Primary polydipsia Arginine-vasopressin Antidiuretic hormone
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