Reference — Endocrine
ADH, SIADH & Diabetes Insipidus Reference
One hormone — antidiuretic hormone (ADH/vasopressin) from the posterior pituitary — controls how much water the kidney keeps. The two disorders are simply too much ADH (SIADH) or too little (DI), and everything else follows.
Educational use only. Fluid management, sodium correction rates, and medications are provider-directed and individualized. This reference is an educational aid. This material supports nursing education and exam review. It is not medical advice and is not a substitute for clinical judgment, institutional policy, or medical direction. Always follow facility protocols and current provider orders.
What ADH Does
ADH is made in the hypothalamus and released from the posterior pituitary when the body senses high osmolality or low volume. It tells the kidney’s collecting ducts to reabsorb water — concentrating the urine and diluting the blood. So ADH = water-retaining hormone. Too much keeps too much water (diluting sodium); too little dumps water (concentrating sodium).
SIADH vs Diabetes Insipidus
| Feature | SIADH (too much ADH) | Diabetes insipidus (too little) |
|---|---|---|
| ADH level | Too MUCH ADH | Too LITTLE ADH (or kidney can't respond) |
| Water | Retained → dilution | Lost → dehydration |
| Serum sodium | LOW (dilutional hyponatremia) | HIGH (hypernatremia) |
| Urine | Concentrated, scant (↑ specific gravity) | Dilute, copious (↓ specific gravity) |
| Serum osmolality | Low | High |
Causes, Types & Treatment
SIADH — causes include small-cell lung cancer (ectopic ADH), CNS disorders, and many drugs (SSRIs, carbamazepine). Treatment: fluid restriction (cornerstone), hypertonic (3%) saline for severe symptomatic hyponatremia given slowly to avoid osmotic demyelination, and vasopressin antagonists (“vaptans”).
Diabetes insipidus — central DI (no ADH made — pituitary/hypothalamic surgery, trauma, tumor) responds to desmopressin (DDAVP); nephrogenic DI (kidney can’t respond to ADH — lithium, hypercalcemia) does not respond to desmopressin and is managed by removing the cause, thiazides, and fluids. The danger in DI is hypovolemia and hypernatremia from massive dilute urine.
NCLEX Pearls
- ✦ADH retains water. SIADH = too much ADH → water retention, LOW sodium, concentrated urine.
- ✦DI = too little ADH → water loss, HIGH sodium, dilute (huge-volume) urine.
- ✦SIADH treatment cornerstone = fluid restriction; DI danger = dehydration/hypernatremia.
- ✦Central DI responds to desmopressin (DDAVP); nephrogenic DI does NOT.
- ✦Correct sodium SLOWLY in both directions — rapid correction risks osmotic demyelination/cerebral edema.
Related Resources
Standards & sources
Fact-checked Jun 20, 2026This page is written to align with American Diabetes Association (ADA) Standards of Care · American Association of Clinical Endocrinology (AACE). It is an educational summary, not a citation of any single document — always verify specific doses, values, and protocols against current guidelines and your facility policy. How we source content →