Diabetes insipidus

The diabetes insipidus ( Syn: Diabetes spurius; Wasserharnruhr ) ( Greek διαβαίνειν diabainein, pass through ' and Latin insipidus, without taste ') is a congenital or acquired disease caused by an increased urine excretion ( polyuria) and increased thirst with increased drinking ( polydipsia ) is characterized.

Forms of diabetes insipidus

Diabetes insipidus centralis

In central diabetes insipidus (syn. diabetes insipidus neurohormonalis ) the cause is a lack or insufficient production of antidiuretic hormone ADH ( Syn: vasopressin ) in the hypothalamus, a lack of transport of ADH by the hypothalamus through the pituitary stalk to the posterior pituitary gland or lack of storage or a lack of secretion of ADH in the posterior pituitary. The ADH acts on the collecting ducts antidiuretisch - so it counteracts the urinary excretion - and leads to the formation of a concentrated urine. For the ADH deficiency a craniocerebral trauma with demolition of the pituitary stalk, a cyst, surgery, inflammation, an infiltrative disease, hemorrhage, infarction, or a tumor of the hypothalamus or the pituitary gland may be responsible. But also a familial diabetes insipidus with a congenital, autosomal dominant hereditary defect is possible as the cause. In one-third of all diabetes insipidus cases the cause is unknown and it is believed an autoimmune disease with autoantibodies against the vasopressin producing cells.

Diabetes insipidus renal

In the rare form of renal (also: nephrogenic ) diabetes insipidus ( ADH or vasopressin Syn - resistant diabetes insipidus ), the defect in the kidney, which can not form a normal concentrated urine despite the presence of the hormone ADH, since the for reabsorption of water from the primary necessary Aquaporinkanal AQP2 is defective or missing, or because the renal tubules are due to chronic kidney disease or drugs (such as lithium) too badly damaged. One speaks here of nephrogenic diabetes insipidus (NDI ) ( nephrogen, starting from the kidney ').

In both forms the kidney differs increasingly from water. If water is not replaced by drinking enough, there is a concentration of sodium in the blood ( hypernatremia ), a so-called hypertonic dehydration.

Diagnostics

• Case history
• Laboratory testing of serum and urine osmolarity
• ADH administration with increase in urine osmolarity at the central diabetes insipidus and lack of increase in renal diabetes insipidus
• When deprivation test the ADH concentration ( antidiuretic hormone, vasopressin ) is measured in the blood plasma or urine after an overnight thirst period; at present diabetes insipidus centralis remains of an increase in ADH. Another test is to be carried out during the Durstens periodic measurements in terms of volume, specific gravity and osmolality of the collected urine. A constant urine volume and low osmolarity are insipidus symptomatic of diabetes. In healthy urine osmolarity weight and get off at physiologically. Instead of ADH copeptin is now measured, since it is easier to measure than ADH.
• Search for the underlying disease

Therapy

Therapeutic approaches are the correction and prevention of any water deficit as well as a reduction of urine loss. In awake patients with an intact thirst, polyuria and polydipsia are often restrictive therefore fix in everyday life and. In comatose patients, however, there is the danger of dehydration and hypernatremia.

When ADH deficiency synthetic ADH is administered ( desmopressin ) daily as a nasal spray, tablet or subcutaneous injection. The ADH enters the blood and with the blood to the kidneys. When renal diabetes insipidus therapy is difficult. Increased fluid intake is mandatory here. In addition, can be helpful because they cause an increased sodium excretion and concentrated urine thiazide diuretics. In particular, in the presence of central diabetes insipidus must be such as tumors of the midbrain, to search for treatable underlying diseases.