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Diabetes insipidus is caused by abnormality in the functioning or levels of antidiuretic hormone (ADH), also known of as vasopressin. Manufactured in the hypothalamus and stored in the pituitary gland, ADH helps to regulate the amount of fluid in the body.
In healthy individuals, when the bodily fluids are depleted, ADH is released from the pituitary gland which prevents the excretion of fluids from the body in the form of urine. ADH acts on the kidneys to increase water permeability in the collecting duct and distal convoluted tubule. Specifically, ADH acts on transmembrane protein channels called aquaporins that open up to allow water into the collecting duct. Once the permeability rises, the water is re-absorbed into the blood, reducing urine volume and increasing its concentration.
In central (cranial) diabetes insipidus, the production or release of ADH is too low to stop the kidneys from passing dilute urine, which results in an increased loss of water and therefore more thirst. People with nephrogenic diabetes insipidus, however, have adequate amounts of ADH in the body but the kidneys fail to respond it, and again the urine is still not concentrated.
Some of the causes of cranial diabetes insipidus include: