What is the 2022 rename and why does it matter in clinical practice?

In 2022, an international consensus group (Christ-Crain et al., *Lancet Diabetes & Endocrinology*) formally recommended renaming the subtypes of diabetes insipidus: 'central DI' becomes **AVP deficiency (AVP-D)**, and 'nephrogenic DI' becomes **AVP resistance (AVP-R)**. The prefix 'diabetes insipidus' was retained as the umbrella term for now, but the subtype names have changed in international specialist literature, endocrinology journals, and some Australian and international guidelines. The renaming matters because it describes the actual pathophysiology — deficient production versus target organ resistance — rather than an anatomical location (central vs peripheral), which can obscure the mechanism and mislead management. In practice, ICD-10 codes have not yet changed (E23.2 and N25.1 remain), so these terms coexist currently. GPs should know both naming conventions and recognise them in specialist correspondence.

How is diabetes insipidus diagnosed — what has replaced the water deprivation test?

The classical water deprivation test (WDT) — withholding fluid for up to 8 hours, then measuring serum and urine osmolality before and after desmopressin — has a diagnostic accuracy of approximately 70–75% for differentiating AVP-D from primary polydipsia (psychogenic polydipsia), and it is poorly tolerated, logistically complex, and can cause severe dehydration. The **copeptin stimulation test** (Christ-Crain et al., *NEJM* 2018) has replaced it in specialist centres. Copeptin is the C-terminal fragment of the pre-pro-AVP peptide, co-secreted with AVP in an equimolar ratio and measurable in plasma with high stability. Copeptin is stimulated using a hypertonic saline infusion (3% NaCl, raising plasma sodium to ~150 mmol/L); measurement at the end of infusion achieves **96% diagnostic accuracy** in a single test. In AVP-D, copeptin fails to rise despite hypertonic stimulation. Copeptin testing is now available in major Australian endocrinology centres (some large public hospitals and private pathology referral laboratories). Until it is universally available, the WDT remains acceptable for initial GP-level workup, but specialist endocrinology review is appropriate for confirmation.

What should happen to desmopressin when a person with AVP-D is admitted to hospital or becomes acutely unwell?

Desmopressin must **not be stopped** in a person with confirmed AVP-D when they are admitted to hospital or become acutely unwell. The omission of desmopressin is a documented cause of severe, life-threatening hypernatraemia. The Atila et al. systematic review (*Lancet Diabetes & Endocrinology*, 2022) analysed hospitalised patients with AVP-D and found that approximately one-third developed hypernatraemia ≥ 150 mmol/L when their desmopressin was withheld, with documented deaths. The NHS England Patient Safety Alert (March 2024) specifically named desmopressin omission as a preventable patient safety incident and recommended: (1) automatic continuation of home desmopressin on admission; (2) prominent flagging of AVP-D diagnosis in admission documentation; (3) pharmacist medication reconciliation on day 1. In Australia, there is no equivalent national alert yet, but GPs should proactively include desmopressin and AVP-D in the hospital referral letter under 'must continue medications.' Provide the patient with a written action card stating 'Do not stop desmopressin when unwell — this will cause dangerous salt imbalance.' If the patient cannot take oral medications when unwell, an IV or subcutaneous desmopressin formulation is available via the treating hospital team.

What is lithium-induced nephrogenic diabetes insipidus (AVP-R) and how is it managed?

Lithium is the most common acquired cause of AVP-R in adults. Approximately 20–40% of patients on long-term lithium develop nephrogenic DI, because lithium accumulates in collecting duct principal cells and downregulates aquaporin-2 water channels — the main targets of AVP signalling. Clinically: polyuria (often 3–10 litres/day), nocturia, polydipsia, urine concentrating defect. Even after lithium cessation, partial AVP-R may persist if tubular damage has occurred. Management: (1) Use the **lowest effective lithium dose** (trough level 0.4–0.6 mmol/L for maintenance, wherever clinically safe with the treating psychiatrist). (2) **Amiloride 5–10 mg daily** is first-line for lithium-induced AVP-R — it blocks ENaC channels in the collecting duct, reducing lithium uptake into tubular cells and partially restoring aquaporin-2. (3) **Thiazide diuretics** (paradoxically reduce polyuria in AVP-R via volume contraction → proximal tubule upregulation) — second-line, but caution with lithium as they raise lithium levels. (4) NSAIDs (indomethacin) can reduce polyuria but interact with lithium toxicity risk and are generally avoided. Joint management with psychiatry is essential before changing lithium dosing.

What are the different desmopressin formulations and which is preferred?

Desmopressin (DDAVP, Minirin) is available in several formulations for AVP-D management in Australia: (1) **Minirin Melt 60 mcg and 120 mcg — sublingual lyophilisate**: preferred for adults. Placed under the tongue, dissolves in 30 seconds, absorbed sublingually — bypasses the first-pass hepatic metabolism and variable gastrointestinal absorption seen with oral tablets. Bioavailability is higher and more predictable than oral tablets. Starting dose typically 60 mcg sublingual at night; titrate to symptom control, usually 60–240 mcg/day in 1–3 divided doses. (2) **Minirin tablets 0.1 mg and 0.2 mg (oral)**: still used in some patients; lower and more variable bioavailability than Melt. (3) **Minirin nasal spray (0.1 mg/mL, 10 mcg per actuation)**: historically first-line; less preferred due to erratic nasal absorption (rhinitis, colds, atrophy affect absorption). Still used in children. (4) **IV / SC desmopressin** (hospital use only, for peri-operative or nil-by-mouth settings). Patients should be counselled on fluid intake restriction while on desmopressin — drinking beyond thirst risks dilutional hyponatraemia. PBS listing: Minirin Melt is PBS-listed under Authority (cranial DI, endocrinology-initiated); the GP can continue a specialist-initiated prescription.

Diabetes insipidus (AVP deficiency / AVP resistance)

Diabetes insipidus (AVP-D/AVP-R): never omit desmopressin in hospital

By Dr HB Lo, FACRRM Reviewed 16 September 2026 9 min read

Diabetes insipidus (DI) causes high-volume dilute urine (> 3–4 L/day) and compensatory thirst. As of 2022, the subtypes are renamed: central DI → **AVP deficiency (AVP-D)**; nephrogenic DI → **AVP resistance (AVP-R)**. Critical hospital safety issue: omitting desmopressin in admitted AVP-D patients causes severe hypernatraemia — ~⅓ develop sodium ≥ 150 mmol/L, with documented deaths (Atila, *Lancet D&E* 2022; NHS England Patient Safety Alert 2024). Diagnosis has shifted from water deprivation testing to **copeptin stimulation** (96% accuracy, Christ-Crain NEJM 2018). Treatment: desmopressin (Minirin Melt sublingual) for AVP-D; amiloride ± thiazide for lithium-induced AVP-R.

Diabetes insipidus — now formally subdivided as AVP deficiency (AVP-D) and AVP resistance (AVP-R) following the 2022 international consensus — is an uncommon but significant endocrine condition that general practice encounters in three main contexts: newly presenting polydipsia-polyuria (diagnosing the cause), ongoing management of known AVP-D (particularly desmopressin safety and hospital handover), and monitoring patients on long-term lithium for developing AVP-R.

This guide covers the 2022 nomenclature update, the diagnostic shift from water deprivation testing to copeptin, the critical desmopressin hospital safety issue, and practical GP management of both subtypes.

A. Core clinical — what every GP needs to know

AVP-D versus AVP-R: pathophysiology in brief

	AVP-D (central DI)	AVP-R (nephrogenic DI)
ICD-10	E23.2	N25.1
Pathophysiology	Deficient AVP production/release from hypothalamus or posterior pituitary	Renal collecting duct resistance to AVP action (aquaporin-2 defect)
AVP/copeptin level	Low or absent (fails to rise with osmotic stimulation)	Elevated or normal (rises appropriately with stimulation)
Response to desmopressin	Yes — urine concentrates	No — urine remains dilute
Common causes	Pituitary surgery, traumatic brain injury, craniopharyngioma, Langerhans cell histiocytosis, idiopathic	Lithium (most common acquired adult cause), hypercalcaemia, hypokalaemia, congenital (X-linked AVPR2 mutation)
Treatment	Desmopressin (Minirin Melt sublingual)	Treat cause; amiloride ± thiazide for lithium-induced AVP-R

Clinical presentation

The hallmark is hypo-osmotic polyuria — large volumes of dilute urine, typically > 3–4 litres/day, with urine osmolality consistently < 300 mOsm/kg (often < 100 mOsm/kg in AVP-D). Patients are persistently thirsty. If thirst mechanism is intact, they maintain serum sodium within or near normal range by compensatory drinking (compensated DI). Neurogenic causes (pituitary surgery, head trauma) may simultaneously impair the thirst centre, resulting in dangerous hypernatraemia.

The GP differential for polyuria includes:

Diabetes mellitus (glucose-driven osmotic diuresis) — fasting glucose/HbA1c first
Primary polydipsia (excessive voluntary water intake suppressing AVP) — most common in psychiatric patients, especially those on medications increasing thirst
AVP-D — usually abrupt onset, often associated with a structural cause
AVP-R — gradual onset, lithium history is the key clue in adults

Initial workup in general practice:

Serum EUC (sodium, potassium, bicarbonate, creatinine)
Plasma osmolality and paired urine osmolality (first morning sample)
Fasting glucose and HbA1c
Serum calcium (hypercalcaemia causes AVP-R)
Serum potassium (hypokalaemia causes AVP-R)
Lithium level (if on lithium)
If urine osmolality < 300 mOsm/kg with serum sodium ≥ 143 mmol/L: refer to endocrinology for formal diagnostic testing (copeptin stimulation)

B. Diagnostic advances — copeptin replaces the water deprivation test

Why the water deprivation test is being phased out

The classical water deprivation test (WDT) requires 8–16 hours of fluid restriction, frequent weight and urine measurements, and desmopressin challenge at the end. It is:

Poorly tolerated (severe thirst, dehydration, potential for dangerous hypernatraemia in AVP-D)
Inaccurate in 25–30% of cases (primary polydipsia patients can partially concentrate urine; AVP-D patients may have partial function)
Labour-intensive and rarely performed well outside specialist centres

Copeptin stimulation test

Copeptin (the C-terminal fragment of pre-pro-AVP) is more stable in plasma than AVP itself and is measurable by a validated immunoassay. Christ-Crain et al. (NEJM 2018) published the landmark trial (n = 156) comparing copeptin after hypertonic saline infusion versus the standard WDT:

Copeptin (post-stimulation cut-off: 4.9 pmol/L) correctly classified 96% of patients versus 70% for WDT
A single stimulated copeptin measurement differentiated AVP-D from primary polydipsia and AVP-R
Baseline (unstimulated) copeptin accurately diagnosed AVP-R (high baseline copeptin in the presence of dilute urine)

Practical note for GPs: Copeptin testing in Australia is available through Laverty Pathology, SA Pathology (Flinders Medical Centre), and Melbourne Pathology (as of 2026) but not universally. The test requires a short IV infusion with sodium monitoring — it is ordered and performed by endocrinologists, not in general practice. GPs should refer patients with confirmed polyuria-polydipsia (urine osmolality < 300 mOsm/kg, serum sodium ≥ 143 mmol/L) to endocrinology rather than attempting a water deprivation test outside a specialist centre.

C. The hospital desmopressin safety alert

The problem: omission causes hypernatraemia and death

When a patient with AVP-D is admitted to hospital, desmopressin must continue on the same schedule as at home. If it is omitted (as a result of nil-by-mouth orders, nursing medication reconciliation gaps, or unfamiliarity with the condition), the patient will immediately begin excreting large volumes of dilute urine. Within 12–24 hours, if intravenous fluid replacement does not keep pace, hypernatraemia develops rapidly. In the Atila et al. systematic review (Lancet Diabetes & Endocrinology, 2022), approximately one-third of hospitalised AVP-D patients who had desmopressin withheld developed plasma sodium ≥ 150 mmol/L; deaths and serious neurological injury were documented.

What the NHS England Patient Safety Alert (2024) recommends

The NHS England alert (March 2024), which represents best practice applicable to Australian hospitals:

Automatic continuation of home desmopressin at admission — treat like insulin or seizure medications
Prominent documentation of AVP-D in the hospital record and medication chart
Pharmacist check on day 1 of admission to ensure desmopressin is charted
Inpatient intravenous or subcutaneous desmopressin available when patient is nil-by-mouth (IV desmopressin 1–4 mcg as equivalent)

GP action

In every referral letter or hospital handover for a patient with AVP-D, include:

“Patient has confirmed AVP deficiency (central DI) and takes desmopressin [dose, timing]. This medication must not be stopped. Omission within 12–24 hours can cause severe hypernatraemia. Please continue or convert to IV/SC desmopressin if oral route unavailable.”

Provide the patient with a written or card-format summary of their condition and the desmopressin non-interruption principle to carry at all times.

D. Lithium and AVP-R: GP monitoring responsibilities

Scope of the problem

Lithium is the most common acquired cause of AVP-R in adult general practice. Among patients on long-term lithium:

20–40% develop some degree of AVP-R (polyuria > 3 L/day)
The risk increases with duration of use and trough lithium levels
Even after lithium cessation, permanent structural tubular damage may persist in some patients

Monitoring for lithium-induced AVP-R

At each lithium monitoring consultation, ask about polyuria and nocturia. If present:

Measure 24-hour urine volume or daytime urine output (voiding diary)
Urine osmolality and paired serum osmolality
Lithium trough level — AVP-R is more likely at higher trough levels
Serum creatinine + eGFR (lithium nephrotoxicity is a broader concern beyond AVP-R)

Management

Dose minimisation: reduce lithium to the lowest effective trough (0.4–0.6 mmol/L for maintenance in bipolar disorder where evidence supports lower levels) — this requires careful collaboration with the treating psychiatrist.
Amiloride 5–10 mg daily: first-line pharmacological treatment for lithium-induced AVP-R. Reduces lithium uptake into collecting duct principal cells, partially restoring aquaporin-2 expression.
Thiazide diuretics (hydrochlorothiazide 12.5–25 mg daily): second-line. Paradoxically reduce polyuria by inducing mild volume contraction → enhanced proximal tubule sodium and water reabsorption, reducing delivery to AVP-unresponsive collecting duct. Caution: thiazides raise serum lithium levels (reduce renal lithium clearance) → monitor lithium levels closely after starting.
NSAIDs (indomethacin): reduce polyuria but raise lithium levels and risk of gastric and renal toxicity — generally avoided.

E. Special populations

Post-pituitary surgery AVP-D

Transsphenoidal pituitary surgery is a common cause of temporary or permanent AVP-D. The triphasic response is characteristic: (1) immediate AVP-D in the first 24–48 hours (AVP neuronal injury); (2) transient SIADH (uncontrolled AVP release from injured neurons, days 4–10, causing hyponatraemia); (3) permanent AVP-D if posterior pituitary stalk or hypothalamic nuclei are damaged. GPs managing patients after pituitary surgery should monitor serum sodium closely in the first two weeks and coordinate with neurosurgery. Do not initiate desmopressin during the SIADH phase (days 4–10) — this can cause dangerous dilutional hyponatraemia.

Pregnancy and AVP-D

Placental vasopressinase degrades AVP rapidly in pregnancy, increasing desmopressin requirements by 2–4-fold. Gestational diabetes insipidus (a distinct entity from chronic AVP-D) occurs in the third trimester when placental vasopressinase overwhelms marginal AVP reserve — it resolves postpartum. Desmopressin is the treatment of choice and is considered safe in pregnancy (it does not cross the placenta to a clinically significant degree). Close sodium monitoring is essential.

Children with AVP-D or AVP-R

Congenital nephrogenic DI (X-linked AVPR2 or autosomal AQPCT mutation) presents in male infants with severe polyuria, failure to thrive, and unexplained fever (hyperthermia from dehydration). These children require paediatric endocrinology management. GPs of affected families should be aware that female carriers of X-linked AVP-R may have variable mild polyuria.

Patients with impaired thirst mechanism (adipsia)

Hypothalamic damage (post-surgery, hypothalamic tumour) can impair both AVP secretion and the thirst centre simultaneously, producing adipsic diabetes insipidus. These patients will not drink compensatorily and are at very high risk of severe hypernatraemia. Fluid prescriptions must be precisely calculated with endocrinology guidance; these patients require daily or twice-daily weight monitoring and a strict fluid protocol.

When to escalate

Emergency (call 000 or send to emergency immediately):

Serum sodium > 155 mmol/L with altered consciousness or haemodynamic instability — hypernatraemic encephalopathy
Severe dehydration in a known AVP-D patient whose desmopressin was interrupted
Hyponatraemia (sodium < 125 mmol/L) in a patient on desmopressin with excessive fluid intake — dilutional hyponatraemia

Urgent endocrinology referral (within 1–2 weeks):

New polyuria-polydipsia with urine osmolality < 300 mOsm/kg and serum sodium ≥ 143 mmol/L — formal diagnostic workup needed
Suspected AVP-D after pituitary surgery or head injury
Serum sodium instability (< 130 or > 150 mmol/L) in a patient on desmopressin

Routine endocrinology referral:

Stable known AVP-D — annual review with GP + endocrinology in alternating years
Lithium-induced AVP-R — collaborative management with psychiatry and endocrinology

What this article is and is not

This article is an evidence-based educational summary for Australian general practitioners, drawing on eTG, AMH, the 2022 international consensus nomenclature, Christ-Crain et al. (NEJM 2018), Atila et al. (Lancet D&E 2022), the NHS England Patient Safety Alert (2024), Endocrine Society of Australia resources, and TGA product information. It is written to help GPs understand the renaming of DI subtypes, the copeptin diagnostic advance, the hospital desmopressin safety imperative, and practical lithium monitoring.

This article does not replace a formal medical consultation, nor does it substitute for the judgment of an endocrinologist managing complex AVP-D or AVP-R cases. Dosing information is current at date of publication; always verify in current eTG, AMH, or PBS before prescribing. Lithium dosing changes should always involve the treating psychiatrist.

No individual is mentioned in this article, and no personal testimonials are cited.

Sources cited

Christ-Crain M et al. — Diagnosis and management of diabetes insipidus for the internist: an update. J Intern Med 2021;290:73–87. onlinelibrary.wiley.com
Christ-Crain M et al. — Copeptin in the differential diagnosis of AVP-dependent disorders. NEJM 2018;379:428–439. nejm.org
Christ-Crain M et al. — Consensus statement on the nomenclature of diabetes insipidus. Lancet Diabetes Endocrinol 2022;10:684–686. thelancet.com
Atila C et al. — Desmopressin omission in hospitalised patients with central DI. Lancet Diabetes Endocrinol 2022;10:750–759. thelancet.com
NHS England — Patient Safety Alert: Desmopressin omission in inpatients with cranial DI (March 2024). england.nhs.uk
eTG — Endocrinology: diabetes insipidus. Therapeutic Guidelines Limited. tg.org.au
AMH — Desmopressin and AVP-D management chapter. Australian Medicines Handbook. amhonline.amh.net.au
Endocrine Society of Australia — Position statement: polyuria-polydipsia and DI evaluation. endocrinology.org.au
TGA — Minirin Melt product information. tga.gov.au
PBS Online — Desmopressin (Minirin Melt) Authority listing. pbs.gov.au
Healthdirect — Diabetes insipidus. healthdirect.gov.au
Better Health Channel — Diabetes insipidus. betterhealth.vic.gov.au
MBS Online — Endocrinology items. mbsonline.gov.au

Frequently asked questions

What is the 2022 rename and why does it matter in clinical practice?

In 2022, an international consensus group (Christ-Crain et al., *Lancet Diabetes & Endocrinology*) formally recommended renaming the subtypes of diabetes insipidus: 'central DI' becomes **AVP deficiency (AVP-D)**, and 'nephrogenic DI' becomes **AVP resistance (AVP-R)**. The prefix 'diabetes insipidus' was retained as the umbrella term for now, but the subtype names have changed in international specialist literature, endocrinology journals, and some Australian and international guidelines. The renaming matters because it describes the actual pathophysiology — deficient production versus target organ resistance — rather than an anatomical location (central vs peripheral), which can obscure the mechanism and mislead management. In practice, ICD-10 codes have not yet changed (E23.2 and N25.1 remain), so these terms coexist currently. GPs should know both naming conventions and recognise them in specialist correspondence.
How is diabetes insipidus diagnosed — what has replaced the water deprivation test?

The classical water deprivation test (WDT) — withholding fluid for up to 8 hours, then measuring serum and urine osmolality before and after desmopressin — has a diagnostic accuracy of approximately 70–75% for differentiating AVP-D from primary polydipsia (psychogenic polydipsia), and it is poorly tolerated, logistically complex, and can cause severe dehydration. The **copeptin stimulation test** (Christ-Crain et al., *NEJM* 2018) has replaced it in specialist centres. Copeptin is the C-terminal fragment of the pre-pro-AVP peptide, co-secreted with AVP in an equimolar ratio and measurable in plasma with high stability. Copeptin is stimulated using a hypertonic saline infusion (3% NaCl, raising plasma sodium to ~150 mmol/L); measurement at the end of infusion achieves **96% diagnostic accuracy** in a single test. In AVP-D, copeptin fails to rise despite hypertonic stimulation. Copeptin testing is now available in major Australian endocrinology centres (some large public hospitals and private pathology referral laboratories). Until it is universally available, the WDT remains acceptable for initial GP-level workup, but specialist endocrinology review is appropriate for confirmation.
What should happen to desmopressin when a person with AVP-D is admitted to hospital or becomes acutely unwell?

Desmopressin must **not be stopped** in a person with confirmed AVP-D when they are admitted to hospital or become acutely unwell. The omission of desmopressin is a documented cause of severe, life-threatening hypernatraemia. The Atila et al. systematic review (*Lancet Diabetes & Endocrinology*, 2022) analysed hospitalised patients with AVP-D and found that approximately one-third developed hypernatraemia ≥ 150 mmol/L when their desmopressin was withheld, with documented deaths. The NHS England Patient Safety Alert (March 2024) specifically named desmopressin omission as a preventable patient safety incident and recommended: (1) automatic continuation of home desmopressin on admission; (2) prominent flagging of AVP-D diagnosis in admission documentation; (3) pharmacist medication reconciliation on day 1. In Australia, there is no equivalent national alert yet, but GPs should proactively include desmopressin and AVP-D in the hospital referral letter under 'must continue medications.' Provide the patient with a written action card stating 'Do not stop desmopressin when unwell — this will cause dangerous salt imbalance.' If the patient cannot take oral medications when unwell, an IV or subcutaneous desmopressin formulation is available via the treating hospital team.
What is lithium-induced nephrogenic diabetes insipidus (AVP-R) and how is it managed?

Lithium is the most common acquired cause of AVP-R in adults. Approximately 20–40% of patients on long-term lithium develop nephrogenic DI, because lithium accumulates in collecting duct principal cells and downregulates aquaporin-2 water channels — the main targets of AVP signalling. Clinically: polyuria (often 3–10 litres/day), nocturia, polydipsia, urine concentrating defect. Even after lithium cessation, partial AVP-R may persist if tubular damage has occurred. Management: (1) Use the **lowest effective lithium dose** (trough level 0.4–0.6 mmol/L for maintenance, wherever clinically safe with the treating psychiatrist). (2) **Amiloride 5–10 mg daily** is first-line for lithium-induced AVP-R — it blocks ENaC channels in the collecting duct, reducing lithium uptake into tubular cells and partially restoring aquaporin-2. (3) **Thiazide diuretics** (paradoxically reduce polyuria in AVP-R via volume contraction → proximal tubule upregulation) — second-line, but caution with lithium as they raise lithium levels. (4) NSAIDs (indomethacin) can reduce polyuria but interact with lithium toxicity risk and are generally avoided. Joint management with psychiatry is essential before changing lithium dosing.
What are the different desmopressin formulations and which is preferred?

Desmopressin (DDAVP, Minirin) is available in several formulations for AVP-D management in Australia: (1) **Minirin Melt 60 mcg and 120 mcg — sublingual lyophilisate**: preferred for adults. Placed under the tongue, dissolves in 30 seconds, absorbed sublingually — bypasses the first-pass hepatic metabolism and variable gastrointestinal absorption seen with oral tablets. Bioavailability is higher and more predictable than oral tablets. Starting dose typically 60 mcg sublingual at night; titrate to symptom control, usually 60–240 mcg/day in 1–3 divided doses. (2) **Minirin tablets 0.1 mg and 0.2 mg (oral)**: still used in some patients; lower and more variable bioavailability than Melt. (3) **Minirin nasal spray (0.1 mg/mL, 10 mcg per actuation)**: historically first-line; less preferred due to erratic nasal absorption (rhinitis, colds, atrophy affect absorption). Still used in children. (4) **IV / SC desmopressin** (hospital use only, for peri-operative or nil-by-mouth settings). Patients should be counselled on fluid intake restriction while on desmopressin — drinking beyond thirst risks dilutional hyponatraemia. PBS listing: Minirin Melt is PBS-listed under Authority (cranial DI, endocrinology-initiated); the GP can continue a specialist-initiated prescription.

Source quality

Sources grouped by evidence tier. AU primary tier first; international where AU is silent or lagging; named-author reconstruction where guidelines have not yet caught up. How tiers work.