AKT · Endocrine/Pituitary & ADH

Diabetes insipidus

ADH deficiency (cranial) or renal ADH resistance (nephrogenic)

Overview

Inability to concentrate urine from lack of ADH (cranial/AVP deficiency — pituitary surgery, tumour, trauma, idiopathic) or renal resistance to ADH (nephrogenic — lithium, hypercalcaemia, hypokalaemia, genetic). Causes large-volume dilute polyuria and intense thirst. The water-deprivation test (then desmopressin) distinguishes the type.

Recognise

Polyuria (large volumes of DILUTE urine) and polydipsia; nocturia; risk of hypernatraemic dehydration if access to water is limited
Dilute urine (low osmolality) despite high/normal plasma osmolality and (often) raised sodium
Cranial: pituitary pathology; Nephrogenic: lithium, hypercalcaemia, hypokalaemia, CKD, genetic

Red flags

Hypernatraemic dehydration (especially if thirst/access impaired — elderly, unconscious) → careful rehydration
Post-pituitary-surgery polyuria → monitor sodium/fluid balance

Differentials & how to tell them apart

Primary polydipsiaexcess water intake; urine concentrates normally on water deprivation, low-normal plasma osmolality

Diabetes mellitusosmotic diuresis with GLYCOSURIA and high glucose

Nephrogenic vs cranial DIresponse to desmopressin — concentrates (cranial) vs no response (nephrogenic)

Investigations

Paired serum/urine osmolality (high serum, low urine osmolality). WATER DEPRIVATION TEST then desmopressin: urine concentrates after desmopressin in CRANIAL DI, but not in NEPHROGENIC DI. Glucose (exclude diabetes mellitus).

Management

Cranial → desmopressin; nephrogenic → remove cause (± thiazide, low-salt diet)

1Confirm with paired osmolalities and the water-deprivation/desmopressin test to separate cranial from nephrogenic and from primary polydipsia. Ensure access to water.Gate: Desmopressin works in CRANIAL DI but not in NEPHROGENIC DI — that response defines the treatment; in nephrogenic DI find and remove the cause (lithium, hypercalcaemia, hypokalaemia)
2Cranial → desmopressin and treat the pituitary cause; nephrogenic → stop the offending drug/correct electrolytes, thiazide + low-salt/protein diet; monitor sodium closely.

Desmopressin (cranial DI) — ADH analogue — replaces the hormone

Treat the cause / thiazide + low-salt (nephrogenic) — stop lithium, correct calcium/potassium; thiazides paradoxically reduce urine volume

Key points

Dilute polyuria + thirst + high-ish sodium = DI. The desmopressin response splits cranial (responds) from nephrogenic (doesn't). Lithium and hypercalcaemia are the classic nephrogenic causes.

Monitor & prognosis

Sodium, fluid balance, urine output.

Good with treatment.

Source: Society for Endocrinology