Last updated:
March 22, 2026
Diabetes insipidus is an inability to concentrate urine due to a lack of antidiuretic hormone (ADH) or insensitivity to ADH in the kidneys.
Classification of diabetes inspidus
| Classification | Description | Causes |
|---|---|---|
| Central diabetes insipidus | Reduced secretion of ADH by the posterior pituitary gland | Idiopathic, tumours, head injury, pituitary surgery, encephalitis, meningitis, Wolfram syndrome (DIDMOAD), mutations in arginine vasopressin-neurophysin II gene (AVP-NPII) |
| Nephrogenic diabetes insipidus | The kidneys are insensitive to ADH | Lithium, hypercalcaemia, hypokalaemia, kidney disease, mutation in vasopressin-2 receptor, mutation in aquaporin-2 gene |
| Gestational diabetes inspidus | Occurs in pregnancy | Increased vasopressinase degrades ADH; increased prostaglandins make the kidneys less sensitive to ADH |
| Dipsogenic diabetes insipidus | Excessive drinking due to impaired thirst mechanism (unquenchable thirst) | Chronic meningitis, multiple sclerosis |
- Signs and symptoms
- Polydipsia
- Polyuria
- Nocturia
- Dehydration
- Focal neurological deficits due to a space-occupying lesion
- Physical examination
- Dry mucous membranes
- Poor skin turgor
- Prolonged capillary refill time
- Tachycardia
- Orthostatic hypotension
- Palpable distended bladder
- Differentials
- Diabetes mellitus
- Psychogenic polydipsia
- Diuretic overuse
- Urinary tract infection
- Hypercalcaemia
- Cushing’s syndrome
- Investigations
- 24-hour urine collection
- Dilute urine
- Plasma osmolality
- Normal plasma osmolality is 285 – 295 mOsmol/kg
- Urine and serum osmolality for the urine to plasma (U:P) osmolality ratio
- Dilute urine with U:P < 2
- Blood glucose to rule out diabetes
- Serum calcium to rule out hypercalcemia
- UECs
- Hypenatremia
- Dilutional hyponatremia may be present in primary polydipsia
- 8-hour water deprivation test: evaluates the kidneys’ ability to concentrate urine. Stage 1 involves fluid deprivation and measuring serum and urine osmolality to evaluate the kidney’s concentrating ability. Stage 2 involves administering desmopressin to differentiate cranial from nephrogenic diabetes insipidus.
- Urine osmolality > 600 mOsmol/kg in stage 1 with a U: P ratio> 2 for normal concentrating ability
- Urine concentrates less than normal in primary polydipsia
- Urine osmolality is increased to > 600 mOsmol/kg after desmopressin
- No increase in urine osmolality after desmopressin in nephrogenic diabetes insipidus
- Serum copeptin – copeptin is a surrogate marker for ADH (it is produced in equimolar amounts from its precursor)
- Low copeptin in central diabetes insipidus
- High copeptin in nephrogenic diabetes insipidus
- 24-hour urine collection
- Treatment
- Correct any underlying causes
- A low-solute diet to reduce osmotic load
- Adequate fluid intake
- Avoid rapid correction of hypernatremia
- Desmopressin for central diabetes insipidus
- Thiazide diuretics (endroflumethiazide) or NSAIDs can be used for nephrogenic diabetes insipidus
- Prostaglandins locally inhibit the action of ADH
- Emergency treatment
- Urgent UECs, serum and urine osmolality
- Monitor serum Na+, urine output and fluid balance
- Intravenous fluids to maintain urine output and to correct hypernatremia
- Trial of desmopressin
Interpretation of the water deprivation test
| Diagnosis | Serum osmolality (mOsm/kg) | Urine osmolality (mOsm/kg) | Urine osmolality after desmopressin given (mOsm/kg) |
|---|---|---|---|
| Normal | 285-295 | >600 | Not completed as normal results |
| Dipsogenic diabetes inspipidus | <300 | 400-600 | No change |
| Cranial diabetic insipidus | >300 | <300 | Urine concentrates following desmopressin administration |
| Nephrogenic diabetes insipidus | >300 | < 300 | No change following desmopressin |