Diabetes Insipidus

• Causes of diabetes insipidus

  • A lack of antidiuretic hormone (cranial diabetes insipidus)
  • A lack of response to antidiuretic hormone (nephrogenic diabetes insipidus)
• Antidiuretic hormone


  Produced in the hypothalamus and secreted by the posterior pituitary gland, also known as vasopressin, stimulates water reabsorption from the collecting ducts in the kidneys
• Symptoms of diabetes insipidus

  • Polyuria (excessive amounts of urine)
  • Polydipsia (excessive thirst)
• Primary polydipsia is when the patient has a normally functioning ADH system but drinks excessive amounts of water, leading to excessive urine production (polyuria). This is not diabetes insipidus.
• Nephrogenic diabetes insipidus is when the collecting ducts of the kidneys do not respond to ADH. It can be idiopathic or caused by medications, genetic mutations, hypercalcaemia, hypokalaemia, or kidney diseases.
• Cranial diabetes insipidus is when the hypothalamus does not produce ADH for the pituitary gland to secrete. It can be idiopathic or caused by brain tumours, brain injury, brain surgery, brain infections, genetic mutations, Wolfram syndrome.
• Presenting features of diabetes insipidus

  • Polyuria (producing more than 3 litres of urine per day)
  • Polydipsia (excessive thirst)
  • Dehydration
  • Postural hypotension
• Investigations for diabetes insipidus

  • Low urine osmolality (lots of water diluting the urine)
  • High/normal serum osmolality (water loss may be balanced by increased intake)
• Symptoms of diabetes insipidus

  • Polyuria (passing more than 3 litres of urine per day)
  • Polydipsia (excessive thirst)
  • Dehydration
  • Postural hypotension
• Water Deprivation Test


  1. The test of choice for diagnosing diabetes insipidus

  2. Also known as the desmopressin stimulation test

  3. The patient avoids all fluids for up to 8 hours before the test (water deprivation)

  4. After water deprivation, urine osmolality is measured

  5. If the urine osmolality is low, synthetic ADH (desmopressin) is given

  6. Urine osmolality is measured over the 2-4 hours following desmopressin
• In primary polydipsia


  • Water deprivation will cause urine osmolality to be high
  • Desmopressin does not need to be given
  • A high urine osmolality after water deprivation rules out diabetes insipidus
• In cranial diabetes insipidus

  • The patient lacks ADH
  • The urine osmolality remains low initially
  • After desmopressin is given, the urine osmolality will be high
• In nephrogenic diabetes insipidus

  • The patient is unable to respond to ADH
  • The urine osmolality will be low both before and after the desmopressin is given
• Urine Osmolality After Water Deprivation

  • Primary Polydipsia: High
  • Cranial Diabetes Insipidus: Low
  • Nephrogenic Diabetes Insipidus: Low
• Urine Osmolality After Desmopressin

  • Primary Polydipsia: Not required
  • Cranial Diabetes Insipidus: High
  • Nephrogenic Diabetes Insipidus: Low
• Management


  1. The underlying cause should be treated (e.g., stopping lithium)

  2. Mild cases may be managed conservatively

  3. Desmopressin (synthetic ADH) can be used in cranial diabetes insipidus to replace the absent antidiuretic hormone

  4. The serum sodium needs to be monitored, as there is a risk of hyponatraemia (low sodium) with desmopressin

  5. Nephrogenic diabetes insipidus is less straightforward to treat

  6. Management options include: Ensuring access to plenty of water, High-dose desmopressin, Thiazide diuretics, NSAIDs