I -Diabetes insipidus (DI)
Diabetes insipidus (DI) may be central or nephrogenic.
Central diabetes insipidus (CDI) is characterized by decreased secretion of antidiuretic hormone (ADH), also known as arginine vasopressin (AVP), that results in polyuria and polydipsia by diminishing the patient's ability to concentrate urine. Diminished or absent ADH can be the result of a defect in one or more sites involving the hypothalamic osmoreceptors, supraoptic or paraventricular nuclei, or the supraopticohypophyseal tract. In contrast, lesions of the posterior pituitary rarely cause permanent diabetes insipidus because ADH is produced in the hypothalamus and still can be secreted into the circulation.
Nephrogenic diabetes insipidus (NDI) is characterized by a decrease in the ability to concentrate urine due to a resistance to ADH action in the kidney.NDI can be observed in chronic renal insufficiency, lithium toxicity, hypercalcemia, hypokalemia, and tubulointerstitial disease; rarely, diabetes insipidus may be hereditary.
II - CDI hay NDI
To distinguish between CDI and NDI, desmopressin stimulation is also used; desmopressin can be taken by injection, a nasal spray, or a tablet.
While taking desmopressin, a patient should drink fluids or water only when thirsty and not at other times, as this can lead to sudden fluid accumulation in the CDI.
If desmopressin reduces urine output and increases osmolarity, the pituitary production of ADH is deficient, and the kidney responds normally.
If the DI is NDI, desmopressin does not change either urine output or osmolarity.
If CDI is suspected, testing of other hormones of the pituitary, as well as magnetic resonance imaging (MRI), is necessary to discover if a disease process (such as a prolactinoma, or histiocytosis,syphilis, tuberculosis or other tumor or granuloma) is affecting pituitary function. Most people with this form have either experienced past head trauma or have stopped ADH production for an unknown reason.