Overview of Water Balance Disorders
| Feature | SIADH | Primary Polydipsia | Diabetes Insipidus (DI) |
|---|---|---|---|
| Pathophysiology | Excess ADH secretion causes water retention | Excess water intake suppresses ADH secretion | Deficiency (central) or resistance (nephrogenic) to ADH |
| Typical causes | CNS disorder, malignancy, drugs | Psychogenic | Central: brain tumour Nephrogenic: drugs, renal disease |
| Serum sodium (baseline) | Hyponatraemia | Hypernatraemia | |
| Serum osmolality (baseline) | Low (<275 mOsm/kg) | High (>295 mOsm/kg) | |
| Urine osmolality (baseline) | High (concentrated) (>100 mOsm/kg) | Low (diluted) (<100 mOsm/kg) | |
| Diagnosis | Diagnosis by exclusion + supported by:
No role of water deprivation test and desmopressin administration |
Detailed fluid intake history
Post-water deprivation test:
Post-desmopressin test:
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Post-water deprivation test:
Post-desmopressin test:
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Some key trends, but presented in a different way:
| Disorder | Trends (at baseline) |
|---|---|
| SIADH |
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| Primary polydipsia |
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| Diabetes insipidus |
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Background Information
Definition
DI is characterised by the excretion of abnormally large volumes of diluted urine.
Pathophysiology
There are 2 types of DI: [Ref1][Ref2]
- Central DI: impaired synthesis / secretion of ADH from the hypothalamus / posterior pituitary
- Nehprogenic DI: resistance to ADH action in the kidney (collecting duct)
Both result in impaired renal water reabsorption, thus inability to concentrate urine and subsequent polyuria.
Aetiology
Central ID is more common than nephrogenic DI.
Both can be hereditary, but it is rare.
Central DI
Main acquired causes: [Ref1][Ref2]
- Idiopathic – most common
- Intracranial tumours (esp. craniopharyngioma)
- Damage to hypothalamus / pituitary stalk (e.g. traumatic brain injury, neurosurgery)
- Infiltrative diseases (e.g. sarcoidosis, Langerhans cell histiocytosis)
Nephrogenic DI
Main acquired causes: [Ref1][Ref2]
- Lithium – most common
- Demeclocycline
- Polycystic kidney disease
- Urethral obstruction
- Electrolyte imbalance (hypercalcaemia, hypokalaemia)
Clinical Features
Key presentation: [Ref1][Ref2]
- Polyuria (nocturia is common)
- Polydipsia
Complication
The main complication is dehydration and hypernatraemia. [Ref1][Ref2]
Investigation and Diagnosis
Step 1 – Biochemical Confirmation
Gold standard: water deprivation test followed by desmopressin administration [Ref1][Ref2]
- The test is aimed at differentiating between central DI vs nephrogenic DI vs primary polydipsia
- Key principle: Interpretation is based primarily on changes in urine osmolality, not serum osmolality
The test is a 3-step process: [Ref1][Ref2]
| Step | Central DI | Nephrogenic DI | Primary polydipsia |
|---|---|---|---|
| Step 1 (baseline) |
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| Step 2 (post-water deprivation) |
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| Step 3 (post-desmopressin administration) |
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Central vs nephrogenic DI:
- Central DI results from deficient ADH production / secretion, therefore by giving desmopressin (a synthetic ADH analogue) will restore ADH’s effect and thus concentrate the urine
- Nephrogenic DI results from renal resistance to ADH (there is no problems with ADH production / secretion), therefore by giving more ADH would not change anything.
Step 2 – Neuroimaging
MRI of the hypothalamic-pituitary region after biochemical confirmation of central DI. [Ref1][Ref2]
Management
Management depends on the type of DI: [Ref]
| Type of DI | Management |
|---|---|
| Central DI |
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| Nephrogenic DI |
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