The following points highlight the two main types of diabetes insipidus. The types are:- 1. Central (Neurogenic) Diabetes Insipi­dus 2. Nephrogenic Diabetes Insipidus.

Type # 1. Central (Neurogenic) Diabetes Insipi­dus:

In central diabetes insipidus, the ADH secretion is poor. Pituitary adenomas rarely causes decrease release of ADH, but hypothalamic tumors such as craniopharyn­giomas or other primary central nervous system lesions and infiltrative or invasive lesions mostly cause damage to the hypotha­lamic pituitary nerve tracts resulting in dis­turbances in the transport of ADH from hypothalamic neurons to neurohypophysis.

These lesions may also damage hypothalam­ic neurons that synthesise ADH. Familial central diabetes insipidus is an autosomal dominant disease that usually occurs in asso­ciation with diabetes mellitus, optic atrophy and deafness.

The primary symptoms of central dia­betes are persistent polyuria and its compan­ions, thirst and polydipsia. The volume of urine may vary from only a few litres per day to a maximum of 18L/day. Most patients have abrupt onset of polyuria and polydipsia in contrast to the slow onset of polyuria due to impaired renal handling of water.

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They usually show a particular predilection for cold or iced drinks to quench thirst. If access to water is interrupted, hypertonic volume depletion develops; these manifestations may cause mental dullness and progressing to coma with secondary signs of ataxia, hyperthermia and hypotension.

Physiologically the plasma osmolality is greater than 287 m mol/L. Serum sodium levels are also elevated and account for the increases in plasma osmolality. In contrast, patients with primary polydipsia have an aberrant thirst mechanism and ingest water independent of physiological stimuli and often have mild dilutional hyponatremia.

Diabetes insipidus, either central or nephro­genic if starts in childhood may impair renal functions due to dilation of urinary bladder, uretus and renal pelvis.

Causes of Neurogenic Diabetes Insipidus:

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i. Hypophysectomy, Complete or Partial

ii. Survey to remove suprasellar tumors

iii. Idiopathic

iv. Familial

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v. Tumors and Cysts

vi. Histiocytosis

vii. Granulomas

viii. Infections

ix. Interruption of Blood Supply

x. Autoimmune

Type # 2. Nephrogenic Diabetes Insipidus:

This type of disease is caused by renal unrespon­siveness to physiologic actions of ADH which is secreted normally. The renal medullary defects as caused by pyelonephritis, poly­cystic disease or cystic disease may prevent formation of a medullary concentration gradi­ent, and, thus, urine passing through the collecting duct system cannot become concen­trated.

Electrolyte disorders like hypokalemia and hypercalcemia reduce urinary concen­tration capacity. Congenital nephrogenic dia­betes is suggested to be X-linked inheritance.

The common picture of this diabetes is volume concentration, hypernatremia and hyperthermia. Mental and physical retar­dation may occur in some children. Urine excreted is always hypnotic to plasma. In some patients, dilation of urinary tract may progress to hydroureter, hydronephrosis and a urinary capacity of more than 1 litre.

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The most characteristic differences of this dia­betes with central diabetes is the absence of thirst and unresponsiveness to administered vasopressin. Renal function is normal as there is no dehydration.

Causes of Nephrogenic Diabetes Insipidius:

i. Chronic renal diseases: Any renal disease that interferes with collecting duct or medullary function, e.g. chronic pyelonephritis.

ii. Hypokalemia

iii. Protein Starvation

iv. Hypercalcemia

v. Sickle cell anaemia

vi. Sjogren’s syndrome

vii. Drugs, e.g. lithium, fluoride, methoxyflurane anesthesia, demeclocycline (Declomycin), colchicine

viii. Congentital defect

ix. Familial

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