Diagnosis
There are essentially two options available for the clinical diagnosis of diabetes insipidus. In both cases the urinosmolarity is measured, i.e. the concentration of urine. On the one hand, the so-called thirst test is available to physicians.
However, this is based on the cooperation of the patient. In the thirst test, which should last a maximum of 24 hours due to fluid loss, there is no increased secretion (excretion) of the hormone ADH despite dehydration (“drying out of the body”). This secretion would be important to ensure that the blood volume is maintained if the fluid intake is too low or absent.
On the other hand, a substance called desmopressin can be administered. This substance has the same function as the hormone vasopressin (ADH). This method can be used to differentiate between central and renal diabetes insipidus.
This is because if no increased urine concentration is detected during the thirst test, diabetes insipidus can be diagnosed, but the exact subtype can only be determined by administering the hormone desmopressin. If the kidney does not react to this, i.e. highly diluted urine is still being excreted, the cause lies in the kidney itself. It is unable to install the water channels. Otherwise, if the concentration of urine is now normal, the cause is central, i.e. in the pituitary gland. Here the pituitary gland produces too little or no ADH (anti-diuretic hormone).
Therapy Diabetes insipidus
The therapy for diabetes insipitus differs depending on the form of the disease. There is diabetes insipitus centralis and diabetes insipitus renalis. In the case of diabetes insipitus centralis, the cause lies in the hypothalamus or in the pituitary gland, whereby the release of ADH (antidiuretic hormone) is disturbed.
In the case of a diabetes insipitus renalis, the cause lies in the kidneys or, more precisely, in the distal tubules and collection tubes. Here the ADH (antidiuretic hormone) can no longer fully develop its effect. The causes of this disorder can be, for example, poisoning or medication as well as renal insufficiency, inflammation of the renal pelvis or even a genetic defect.
Depending on the classification of the disease, therapies must have different approaches in order to be effective. In both therapy approaches, the aim is to compensate for an imminent water deficit in the body and to reduce urine loss. This is achieved by different approaches.
1) The therapy of diabetes insipitus centralis is considered to be simpler, since desmopressin (vasopressin analogue) is administered. Desmopressin is an antidiuretic, i.e. a drug that reduces urinary excretion. Desmopressin is an analogue of the antidiuretic hormone, an endogenous hormone that stimulates the tubules of the kidneys to let more water through.
As a result, more water is reabsorbed and less urine excreted. This urine is then more concentrated. Since ADH (antidiuretic hormone) is no longer released in the case of diabetes insipitus centralis due to a disorder in the hypothalamus and pituitary gland, therapy intervenes here by taking over the function of ADH with the desmopressin administered.
This desmopressin can be administered orally (solution) or nasally (nasal spray). 2. however, therapy for diabetes insipitus renalis is somewhat more difficult. Thiazide diuretics can be given.
Thiazide diuretics belong to the so-called diuretic agents. They act on the distal tubules of the kidneys and ensure an increased excretion of sodium. This makes the excreted urine more concentrated. In addition, an increased intake of fluid is obligatory in the case of diabetes insipitus renalis.