The patients of diabetes insipidus present to the hospital with the complaint of polyuria and/or dehydration. The patient may pass 5 to 20 or even more liters of urine in 24 hours. The urine has a very low specific gravity and osmolality.

As the patient loses a lot of water, signs of dehydration start appearing. The mouth becomes dry and the skin loses its elasticity. The patient also has excessive thirst (polydipsia).

The diagnosis of diabetes insipidus is established by the use of the following investigations [6].

• Plasma osmolality: Since the amount of antidiuretic hormone is not measurable in the serum, the osmolality of the plasma is tested. It is significantly raised in diabetes insipidus. A plasma osmolality greater than 300 mOsm/kg is diagnostic of diabetes insipidus.
• Urine osmolality: The osmolality of the urine is less than 600 mOsm/kg in diabetes insipidus.
• Water deprivation test: The objective of water deprivation test is to establish the diagnosis of diabetes insipidus and to determine whether the cause is central or nephrogenic. In central diabetes insipidus, the osmolality of urine increases from less than 600 mOsm/kg to over 660 mOsm/kg after the administration of desmopressin, an analogue of anti-diuretic hormone. In nephrogenic diabetes insipidus, the concentration of the urine remains the same even after the administration of desmopressin.

Rehydration

The patients suffering from diabetes insipidus have to be rehydrated with intravenous or oral fluids depending upon their severity of dehydration.

Central diabetes insipidus

An analog of antidiuretic hormone called desmopressin is the treatment of choice for central diabetes insipidus. The bioavailability of desmopressin in oral form is negligible. Therefore, it is usually given in the form of nasal spray. It may also be given intramuscularly if the patient is acutely ill [7].

Nephrogenic diabetes insipidus

Thiazide diuretics have a paradoxical effect and decrease polyuria in both central and nephrogenic diabetes insipidus. A combination of indomethacin and hydrochlorothiazide or indomethacin and amiloride may be used in nephrogenic diabetes [8] [9] [10]. In addition, the use of low salt diet may be advised to reduce thirst and to lower the excretion of water.

With proper treatment, the prognosis for the people suffering from diabetes insipidus is excellent. Central diabetes insipidus responds to treatment much more easily than nephrogenic diabetes insipidus.

Although the patients of diabetes insipidus rapidly become dehydrated, mortality from it is rare in previously healthy adult patients. Children and the elderly are at a higher risk of mortality from severe dehydration.

Diabetes insipidus is of two types, central and nephrogenic.

Central diabetes insipidus

Central diabetes insipidus results from deficient production of antidiuretic hormone (ADH) in the hypothalamus or their inability to reach the posterior pituitary from where they are released in the blood [1]. It is most commonly associated with hypothalamic or high stalk lesions such as craniopharyngioma, sarcoidosis, histiocytosis X, tuberculous meningitis, encephalitis and syphilis [2]. Head injuries and surgeries may also cause damage to the hypothalamus. Pituitary tumors with suprasellar extension or metastases to the pituitary may also cause central diabetes insipidus. Central diabetes insipidus may also have idiopathic or genetic etiologies [3].

Nephrogenic diabetes insipidus

It results from the lack of response of renal tubules to antidiuretic hormone [4]. It is associated with renal damage with may result from genetic defects (sex linked recessive defects, cystinosis), metabolic abnormalities (such as hypokalemia and hypercalcemia), drug therapy (with lithium or demeclocycline) or heavy metal poisoning. It may also be caused by other conditions such as pyelonephritis, renal amyloidosis, multiple myeloma and Sjogren syndrome.

Not much data is available regarding the epidemiology of diabetes insipidus. However, it is a rare disease with a prevalence of 3 per 100,000 people in the United States [5]. The prevalence is equal in men and women. Various ethnic groups also have equal tendencies for the development of diabetes insipidus.

Antidiuretic hormone is a nonpeptide hormone that is formed in the hypothalamus and stored in the posterior pituitary. Its primary effect is on the epithelial cells of the renal collecting tubules where it augments the resorption of water independently of the solutes. This causes dilution of the blood serum and concentration of the urine.

Diabetes insipidus results due to a decreased effect of antidiuretic hormone. The cause may be central or nephrogenic. Central diabetes insipidus results from an ineffective production of antidiuretic hormone; whereas in nephrogenic diabetes insipidus, the cells of the kidney fail to respond to it.

There are no documented ways to prevent the development of diabetes insipidus.

Diabetes insipidus is an endocrine disease characterized by the persistent excretion of excessive quantities of dilute urine and constant, excessive thirst. It results from a decreased action of antidiuretic hormone - the posterior pituitary hormone that is responsible for the suppression of urination by increasing the resorption of water in the renal collecting tubules. It may be due to a decreased production of antidiuretic hormone or the inability of the renal cells to respond to it.

Diabetes insipidus is treated by the administration of desmopressin (an analog of antidiuretic hormone) along with thiazide diuretics. The disease is fatal unless adequate rehydration and proper treatment is ensured.

The pituitary gland is a small gland located at the base of the brain. One of the hormone it secretes is called antidiuretic hormone. This hormone acts on the kidneys and causes absorption of water back into the blood, thereby preventing the excessive loss of water in the urine. In diabetes insipidus, there is either a reduced production or inadequate effect of antidiuretic hormone which causes the loss of a large amount of water in the urine. The patients develop dehydration and excessive thirst. With proper treatment, there is an excellent control of the disease.

1. Gu F, Jin Z, Zhang D. [The etiology and clinical characteristics of central diabetes insipidus, a retrospective study of 408 cases]. Zhonghua yi xue za zhi. Oct 2001;81(19):1166-1171.
2. Garcia Garcia E, Lopez Siguero JP, Milano Manso G, Martinez Valverde A. [Etiology of central diabetes insipidus in children]. Anales espanoles de pediatria. Jul 1999;51(1):53-55.
3. Babey M, Kopp P, Robertson GL. Familial forms of diabetes insipidus: clinical and molecular characteristics. Nature reviews. Endocrinology. Dec 2011;7(12):701-714.
4. Earley LE, Orloff J. The Mechanism of Antidiuresis Associated with the Administration of Hydrochlorothiazide to Patients with Vasopressin-Resistant Diabetes Insipidus. The Journal of clinical investigation. Nov 1962;41(11):1988-1997.
5. Saborio P, Tipton GA, Chan JC. Diabetes insipidus. Pediatrics in review / American Academy of Pediatrics. Apr 2000;21(4):122-129; quiz 129.
6. Laczi F. [Diabetes insipidus: etiology, diagnosis, and therapy]. Orvosi hetilap. Nov 17 2002;143(46):2579-2585.
7. Laczi F. [Treatment of diabetes insipidus]. Orvosi hetilap. Mar 28 2004;145(13):699-702.
8. Allen HM, Jackson RL, Winchester MD, Deck LV, Allon M. Indomethacin in the treatment of lithium-induced nephrogenic diabetes insipidus. Archives of internal medicine. May 1989;149(5):1123-1126.
9. Finch CK, Kelley KW, Williams RB. Treatment of lithium-induced diabetes insipidus with amiloride. Pharmacotherapy. Apr 2003;23(4):546-550.
10. Alon U, Chan JC. Hydrochlorothiazide-amiloride in the treatment of congenital nephrogenic diabetes insipidus. American journal of nephrology. 1985;5(1):9-13.