Definition
Diabetes insipidus (DI) is the passage of large volumes of dilute urine due to a problem with antidiuretic hormone (ADH, vasopressin):
- Cranial DI — deficient ADH production
- Nephrogenic DI — renal resistance to ADH
Causes
Cranial: idiopathic, pituitary/hypothalamic tumours, trauma, neurosurgery, infiltration (sarcoidosis, histiocytosis), haemorrhage.
Nephrogenic: lithium, hypercalcaemia, hypokalaemia, chronic kidney disease, and genetic defects (AVPR2 receptor, aquaporin-2).
Clinical presentation
- Polyuria and polydipsia, nocturia
- Dilute urine with a low urine osmolality
- Hypernatraemia if access to water is limited
Investigations
- High or high-normal plasma osmolality with inappropriately dilute urine
- Water deprivation test: urine fails to concentrate on fluid restriction; then give desmopressin —
- Cranial: urine osmolality rises (responds)
- Nephrogenic: urine osmolality does not rise
- Investigate the underlying cause (pituitary MRI, calcium, drug review)
Management
- Cranial DI: desmopressin (a synthetic ADH analogue)
- Nephrogenic DI: treat the cause (stop lithium, correct calcium/potassium); thiazide diuretics and a low-salt/low-protein diet paradoxically reduce urine output
MRCP-specific traps
- Lithium is the classic drug cause of nephrogenic DI.
- Primary polydipsia also causes dilute polyuria but concentrates normally on water deprivation.
- Distinguish DI (dilute urine) from osmotic diuresis in diabetes mellitus (glycosuria).
Summary
DI is dilute polyuria from ADH deficiency (cranial) or resistance (nephrogenic, classically lithium/hypercalcaemia). The water deprivation test with desmopressin separates them: cranial concentrates with desmopressin, nephrogenic does not. Treat cranial with desmopressin; treat the cause plus thiazides in nephrogenic.
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