Diabetes Insipidus



Diabetes insipidus is a lack of antidiuretic hormone (ADH) or a lack of response to ADH. This prevents the kidneys from being able to concentrate the urine leading to polyuria (excessive amounts of urine) and polydipsia (excessive thirst). It can be classified as nephrogenic or cranial.

Primary polydipsia is when the patient has a normally functioning ADH system but they are drinking excessive quantities of water leading to excessive urine production. They don’t have diabetes insipidus.

 

Nephrogenic Diabetes Insipidus

Nephrogenic diabetes insipidus is when the collecting ducts of the kidneys do not respond to ADH. It can also be caused by:

  • Drugs, particularly lithium used in bipolar affective disorder
  • Mutations in the AVPR2 gene on the X chromosome that codes for the ADH receptor
  • Intrinsic kidney disease
  • Electrolyte disturbance (hypokalaemia and hypercalcaemia)

 

Cranial Diabetes Insipidus

Cranial diabetes insipidus is when the hypothalamus does not produce ADH for the pituitary gland to secrete. It can be idiopathic, without a clear cause or it can be caused by:

  • Brain tumours
  • Head injury
  • Brain malformations
  • Brain infections (meningitis, encephalitis and tuberculosis)
  • Brain surgery or radiotherapy

 

Presentation

  • Polyuria (excessive urine production)
  • Polydipsia (excessive thirst)
  • Dehydration
  • Postural hypotension
  • Hypernatraemia

 

Investigations

  • Low urine osmolality
  • High serum osmolality
  • Water deprivation test

 

Water Deprivation Test

The water deprivation test is also known as the desmopressin stimulation test. This is the test of choice for diagnosing diabetes insipidus.

Method

Initially the patient should avoid taking in any fluids for 8 hours. This is referred to as fluid deprivation. Then, urine osmolality is measured and synthetic ADH (desmopressin) is administered. 8 hours later urine osmolality is measured again.

Results

In cranial diabetes insipidus the patient lacks ADH. The kidneys are still capable of responding to ADH. Therefore initially the urine osmolality remains low as it continues to be diluted by excessive water secretion in the kidneys. Then when synthetic ADH is given the kidneys respond by reabsorbing water and concentrating the urine so the urine osmolality will be high.

In nephrogenic diabetes insipidus the patient is unable to respond to ADH. They are diluting their urine with the excessive water secretion by the kidneys. Therefore the urine osmolality will be low initially and remain low even after the synthetic ADH is given.

In primary polydipsia the 8 hours of water deprivation will cause the urine osmolality to be high even before the synthetic ADH is given. A high urine osmolality after 8 hours of water deprivation indicates no diabetes insipidus.

Diagnosis

After Deprivation

After ADH

Cranial Diabetes Insipidus

Low

High

Nephrogenic Diabetes Insipidus

Low

Low

Primary Polydipsia

High

High

 

Management

If possible, treat underlying cause. Mild cases can be managed conservatively without any intervention.

Desmopressin (synthetic ADH) can be used in:

  • Cranial diabetes insipidus to replace ADH
  • Nephrogenic diabetes insipidus in higher doses under close monitoring

 

Last updated December 2018
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