Hypernatraemia (High Sodium) Cause Interpreter
Hypernatraemia (High Sodium) Cause Interpreter
Find the cause of a high sodium from the urine. Enter the urine osmolality and the 24-hour urine volume, and the response to desmopressin if it was given. The page separates water lost outside the kidney or never drunk, an osmotic diuresis (with the osmolar excretion worked out), and diabetes insipidus — now called AVP deficiency and AVP resistance under the 2022 renaming.
Why is the sodium high?
Sodium, urine osmolality and volume, desmopressin → causeAn 80 kg man in intensive care on a high-protein tube feed. Sodium 154 mmol/L, urine osmolality 420 mOsm/kg, urine output 4.2 L over 24 hours. No desmopressin given.
The steps
Urine osmolality 800 mOsm/kg or more → kidney concentrating: extrarenal loss, low intake or sodium gain
Below 300 mOsm/kg → AVP deficiency or AVP resistance: desmopressin rise above 50% → deficiency; below 10% → resistance
300 to 800 → osmolar excretion = urine osmolality × 24-h volume: above 1,000 mOsm/day → osmotic diuresis; otherwise partial AVP deficiency or resistance
- osmolar excretion
- urine osmolality (mOsm/kg) × urine volume (L/day), taking 1 L of urine as 1 kg; about 600 to 900 mOsm a day on a normal diet
- AVP deficiency / AVP resistance
- the 2022 names for central and nephrogenic diabetes insipidus
- 800 vs 600
- Yun 2023 and the water deprivation test use 800 mOsm/kg as full concentration; Medscape’s workup accepts extrarenal loss above 600
Worked example
An 80 kg man in intensive care on a high-protein tube feed. Sodium 154 mmol/L, urine osmolality 420 mOsm/kg, urine output 4.2 L over 24 hours. No desmopressin given.
Sodium 154 is above 145 → hypernatraemia
Urine osmolality 420 is between 300 and 800 → neither dilute nor maximally concentrated
Osmolar excretion = 420 × 4.2 = 1,764 mOsm/day, well above 1,000
→ osmotic diuresis; the feed's protein becomes urea, and the urea carries the water out
Urine osmolality in hypernatraemia
| Urine osmolality | What it means | Usual causes |
|---|---|---|
| 800 mOsm/kg or more | Kidney concentrating fully | Insensible, sweat or gut water loss; no access to water; hypodipsia; sodium gain |
| 300 to 800 | Submaximal | Osmotic diuresis (osmolar excretion above 750–1,000 mOsm/day), partial AVP deficiency or resistance, AVP deficiency with volume depletion |
| Below 300 | Inappropriately dilute | AVP deficiency or AVP resistance |
The 2022 renaming
| Old name | New name |
|---|---|
| Central (cranial) diabetes insipidus | Arginine vasopressin deficiency (AVP-D) |
| Nephrogenic diabetes insipidus | Arginine vasopressin resistance (AVP-R) |
The urine answers the question the sodium cannot
A high sodium almost always means too little water rather than too much sodium, and a patient who can feel thirst and reach water rarely becomes hypernatraemic. So the question is where the water went, and the urine answers it. A high sodium is the strongest possible stimulus for vasopressin, so a healthy kidney should be making small volumes of concentrated urine. If it is, at 800 mOsm/kg or more, the kidney is not the problem: the water was lost through skin, lungs or gut, or never drunk. If the urine is dilute, below 300 mOsm/kg, the kidney is losing water it should be keeping.
Between the two is the zone where most intensive care patients sit, and the useful number there is not the osmolality but the osmolar excretion — osmolality times the day’s urine volume. A normal diet produces about 600 to 900 mOsm of solute a day. When the kidney is excreting well over 1,000, a solute is driving the diuresis: glucose, mannitol, or urea from a high-protein feed or from the catabolism of critical illness. That last one is easily missed, because the urine is neither dilute nor concentrated and nobody has named a solute.
Dilute urine at a high sodium is diabetes insipidus, which since 2022 has two new names: arginine vasopressin deficiency (AVP-D) for the central form and arginine vasopressin resistance (AVP-R) for the nephrogenic form. An international working group proposed the change because the shared word diabetes had caused confusion with diabetes mellitus, and patients had died when desmopressin was withheld. Desmopressin separates the two: a rise in urine osmolality of more than 50% points to deficiency, less than 10% to resistance.
There is no formal guideline for the diagnosis of hypernatraemia, and published cut-offs differ; this page uses the 300 and 800 mOsm/kg figures that the water deprivation test interpreter also uses, and shows where others differ. Calculate the water to replace with the free water deficit calculator, and see the copeptin interpreter for the tests that separate the forms of AVP deficiency. This page supports clinical judgement and does not replace it.
Frequently asked questions
What urine osmolality suggests diabetes insipidus in hypernatraemia?
Below 300 mOsm/kg. A high sodium should make the kidney concentrate the urine, so dilute urine means AVP deficiency (central) or AVP resistance (nephrogenic).
What is the new name for diabetes insipidus?
Arginine vasopressin deficiency (AVP-D) for central diabetes insipidus and arginine vasopressin resistance (AVP-R) for nephrogenic, proposed by an international working group in 2022.
How do I recognise an osmotic diuresis?
Multiply the urine osmolality by the 24-hour urine volume. Yun and colleagues put an osmotic diuresis at an osmolar excretion above 750 to 1,000 mOsm a day. Glucose, urea and mannitol are the usual solutes.
What desmopressin response separates central from nephrogenic?
A rise in urine osmolality of more than 50% points to AVP deficiency (central). Less than 10% points to AVP resistance (nephrogenic). Between 10% and 50% is indeterminate.
Is a concentrated urine reassuring?
For the kidney, yes: 800 mOsm/kg or more means vasopressin and the kidney are working. The water was lost elsewhere or not drunk, or sodium was added. Some reviews accept 600 mOsm/kg as enough.
Related calculators
References
- Yun G, Baek SH, Kim S. Evaluation and management of hypernatremia in adults: clinical perspectives. Korean J Intern Med. 2023;38(3):290–302.
- Lukitsch I. Hypernatremia workup. Medscape Reference. Updated 3 January 2023.
- Arima H, Cheetham T, Christ-Crain M, et al; Working Group for Renaming Diabetes Insipidus. Changing the name of diabetes insipidus: a position statement. Endocr Connect. 2022;11(11):e220378. Published simultaneously in Eur J Endocrinol, J Clin Endocrinol Metab, Endocr J, Clin Endocrinol, Pituitary, Arch Endocrinol Metab and Horm Res Paediatr.
- Adrogué HJ, Madias NE. Hypernatremia. N Engl J Med. 2000;342(20):1493–1499.
Not medical advice. For healthcare professionals and education. Reference intervals vary by laboratory and assay — always use your own laboratory's. Never base a dose or a treatment decision on this page alone. Full disclaimer at calcengines.com/disclaimer/