Syndrome of inappropriate antidiuretic hormone secretion (SIADH)

Last updated: June 10, 2025

Syndrome of inappropriate antidiuretic hormone secretion (SIADH)

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Anemia: Clinical
Microcytic anemia: Pathology review
Non-hemolytic normocytic anemia: Pathology review
Intrinsic hemolytic normocytic anemia: Pathology review
Extrinsic hemolytic normocytic anemia: Pathology review
Macrocytic anemia: Pathology review
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Endocrine system anatomy and physiology
Risk factors for periodontitis
Anatomy of the thyroid and parathyroid glands
Diabetes mellitus: Clinical
Hyperthyroidism: Clinical
Hypothyroidism and thyroiditis: Clinical
Parathyroid conditions and calcium imbalance: Clinical
Thyroid nodules and thyroid cancer: Clinical
Pituitary adenomas and pituitary hyperfunction: Clinical
Hypopituitarism: Clinical
Cushing syndrome: Clinical
Adrenal masses and tumors: Clinical
MEN syndromes: Clinical
Hyperthyroidism medications
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Insulins
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Adrenal hormone synthesis inhibitors
Mineralocorticoids and mineralocorticoid antagonists
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HIV (AIDS)
Human herpesvirus 8 (Kaposi sarcoma)
Chronic kidney disease: Clinical
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Obstructive lung diseases: Pathology review
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Syncope: Clinical
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Hypertension: Clinical
Hypercholesterolemia: Clinical
Sympatholytics: Alpha-2 agonists
Adrenergic antagonists: Presynaptic
Adrenergic antagonists: Alpha blockers
Adrenergic antagonists: Beta blockers
ACE inhibitors, ARBs and direct renin inhibitors
Thiazide and thiazide-like diuretics
Calcium channel blockers
cGMP mediated smooth muscle vasodilators
Class I antiarrhythmics: Sodium channel blockers
Class II antiarrhythmics: Beta blockers
Class III antiarrhythmics: Potassium channel blockers
Class IV antiarrhythmics: Calcium channel blockers and others
Lipid-lowering medications: Statins
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Osteogenesis imperfecta
Acyanotic congenital heart defects: Pathology review
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Cardiomyopathies: Pathology review
Heart failure: Pathology review
Systemic lupus erythematosus (SLE): Clinical
Diabetic retinopathy
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Congenital adrenal hyperplasia
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Waterhouse-Friderichsen syndrome
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Cushing syndrome
Conn syndrome
Thyroglossal duct cyst
Hyperthyroidism
Graves disease
Thyroid eye disease (NORD)
Toxic multinodular goiter
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Hypothyroidism
Euthyroid sick syndrome
Hashimoto thyroiditis
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Thyroid cancer
Hyperparathyroidism
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Hypercalcemia
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Diabetes mellitus
Hyperpituitarism
Pituitary adenoma
Hyperprolactinemia
Prolactinoma
Gigantism
Acromegaly
Hypopituitarism
Pituitary apoplexy
Sheehan syndrome
Hypoprolactinemia
Constitutional growth delay
Diabetes insipidus
Syndrome of inappropriate antidiuretic hormone secretion (SIADH)
Precocious puberty
Delayed puberty
Premature ovarian failure
Polycystic ovary syndrome
Androgen insensitivity syndrome
Kallmann syndrome
5-alpha-reductase deficiency
Autoimmune polyglandular syndrome type 1 (NORD)
Multiple endocrine neoplasia
Pancreatic neuroendocrine neoplasms
Zollinger-Ellison syndrome
Pheochromocytoma
Neuroblastoma
Opsoclonus myoclonus syndrome (NORD)
Adrenal insufficiency: Pathology review
Adrenal masses: Pathology review
Hyperthyroidism: Pathology review
Hypothyroidism: Pathology review
Thyroid nodules and thyroid cancer: Pathology review
Parathyroid disorders and calcium imbalance: Pathology review
Diabetes mellitus: Pathology review
Cushing syndrome and Cushing disease: Pathology review
Pituitary tumors: Pathology review
Hypopituitarism: Pathology review
Diabetes insipidus and SIADH: Pathology review
Multiple endocrine neoplasia: Pathology review
Immune thrombocytopenia
Mixed platelet and coagulation disorders: Pathology review
Hypertension
Heparin-induced thrombocytopenia
Raynaud phenomenon
Nephritic syndromes: Pathology review
Down syndrome (Trisomy 21)
Rett syndrome
Restrictive lung diseases: Pathology review
Sarcoidosis
Parkinson disease
Cranial nerves
Spina bifida
Chiari malformation
Dandy-Walker malformation
Syringomyelia
Tethered spinal cord syndrome
Aqueductal stenosis
Septo-optic dysplasia
Cerebral palsy
Spinocerebellar ataxia (NORD)
Transient ischemic attack
Ischemic stroke
Intracerebral hemorrhage
Epidural hematoma
Subdural hematoma
Subarachnoid hemorrhage
Saccular aneurysm
Arteriovenous malformation
Broca aphasia
Wernicke aphasia
Wernicke-Korsakoff syndrome
Kluver-Bucy syndrome
Concussion and traumatic brain injury
Shaken baby syndrome
Seizures and epilepsy
Febrile seizure
Early infantile epileptic encephalopathy (NORD)
Tension headache
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Migraine
Idiopathic intracranial hypertension
Trigeminal neuralgia
Cavernous sinus thrombosis
Alzheimer disease
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Normal pressure hydrocephalus
Torticollis
Essential tremor
Restless legs syndrome
Parkinson disease
Huntington disease
Multiple sclerosis
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Acute disseminated encephalomyelitis
Transverse myelitis
JC virus (Progressive multifocal leukoencephalopathy)
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Brown-Sequard Syndrome
Cauda equina syndrome
Treponema pallidum (Syphilis)
Vitamin B12 deficiency
Friedreich ataxia
Neurogenic bladder
Meningitis
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Brain abscess
Epidural abscess
Sturge-Weber syndrome
Tuberous sclerosis
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Spinal muscular atrophy
Poliovirus
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Charcot-Marie-Tooth disease
Bell palsy
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Thoracic outlet syndrome
Carpal tunnel syndrome
Ulnar claw
Erb-Duchenne palsy
Klumpke paralysis
Sciatica
Myasthenia gravis
Lambert-Eaton myasthenic syndrome
Orthostatic hypotension
Horner syndrome
Congenital neurological disorders: Pathology review
Headaches: Pathology review
Seizures: Pathology review
Cerebral vascular disease: Pathology review
Traumatic brain injury: Pathology review
Spinal cord disorders: Pathology review
Dementia: Pathology review
Central nervous system infections: Pathology review
Movement disorders: Pathology review
Neuromuscular junction disorders: Pathology review
Demyelinating disorders: Pathology review
Adult brain tumors: Pathology review
Pediatric brain tumors: Pathology review
Neurocutaneous disorders: Pathology review

Transcript

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Content Reviewers

How does your body know when to retain fluids and when to get rid of them?

It’s not like you just think to yourself “I’ve had too much water, better get rid of some.” (If you do, and it works, call us).

Your body uses chemicals called hormones to send widespread messages, kind of like how the P.A. system at school tells everyone to ignore the smoke billowing out of the science wing.

The antidiuretic hormone, abbreviated as ADH, is the hormone that controls water retention in the body.

It also constricts blood vessels, and incidentally the vasoconstrictor drug called vasopressin is just ADH. Cool! But that’s not what we’re talking about right now.

Anyways, the more ADH floating around in your blood, the more fluid you retain.

The less ADH in your blood, the more fluid you excrete.

The nephrons in the kidneys are the structures that physically control how much water is excreted from your body.

Nephrons are mostly a series of tubes attached end-to-end that type fluids and wastes towards the bladder.

These tubes though also allow fluids and electrolytes to move through the tube walls and back into the blood if needed.

ADH affects the last two-thirds of these tubes, called the distal convoluted tubule and the collecting ducts.

These tubes focus almost exclusively on reabsorbing water back into the blood.

The wall of these tubes are unsurprisingly made up of cells, a common trait of living things, but these cells have proteins called aquaporins.

Aquaporins allow water to move quickly in and out of the cells.

The more ADH floating around in the blood, the more aquaporins are available to... ahem...facilitate water movement through the cell (yo, wata, come over here for a sec).

So when ADH is low, most of the water flows through the distal convoluted tubule and the collecting duct, giving us diluted urine.

When ADH is high, aquaporins grab much of the water passing through the these tubes and throws them back into the blood.

When I drink a glass of water and that water is absorbed into my blood, my plasma osmolality drops, which means I’m diluting my blood with the water.

That means there’s more fluid for all those blood cells to bounce around in (wooo parrttayy).

The part of my brain called the hypothalamus sees this drop in plasma osmolality and tells the pituitary gland to slow down the release of ADH (that’s enough!).

Low ADH leads to lots of diluted urine (urine with low osmolality), which brings our plasma osmolality back to normal. What a nifty feedback loop.

Now suppose ADH continues to be released even though my plasma osmolality has dropped (stop it! STOP IT! pituitary gland whistling).

We’re going to continue retaining water, and as we drink more and more water, we might expect our plasma osmolality to continue dropping. However this isn’t exactly the case.

As more water is retained, it dilutes the other solutes floating around in our blood, like sodium.

The extra fluid also takes up more space in our blood vessels.

This taking up more space issue triggers another mechanism in our body that causes the hormone aldosterone to stop being released.

Less aldosterone floating around in the blood causes the body to start dumping sodium from the blood into the urine.

Concentration gradients cause water to follow sodium, so we end up with the excess water being excreted in the urine with the sodium, normalizing the fluid volume in the blood.

So now our body is removing sodium from blood that already has a lower concentration of sodium. Uh oh!

This means the plasma sodium osmolarity is dropping significantly.

This whole fiasco we’ve just talked about is called syndrome of inappropriate antidiuretic hormone, often abbreviated as SIADH.

Key Takeaways

Syndrome of inappropriate antidiuretic hormone secretion (SIADH) is characterized by excessive release of antidiuretic hormone from the posterior pituitary gland or another source. The increase in fluid retention often results in dilutional hyponatremia in which the plasma sodium levels are lowered. SIADH may present with euvolemic hyponatremia with continued urinary sodium excretion. Urine osmolality is usually higher than serum osmolality. Very low serum sodium levels can lead to cerebral edema or seizures. Other symptoms of SIADH include fatigue, confusion, muscle weakness, nausea, vomiting, lack of appetite, and weight loss. Treatment usually involves fluid restriction, salt tablets, IV hypertonic saline, diuretics, and drugs like conivaptan, tolvaptan, or demeclocycline.