Vasopressin (ADH) Unit Converter
Vasopressin (ADH) Unit Converter
Convert arginine vasopressin between pg/mL, ng/L and pmol/L — and read why AVP is so unstable ex vivo that copeptin, its equimolar precursor fragment, has largely replaced it.
Vasopressin (ADH) converter
Mass ⇄ molarAVP 2.5 pg/mL, drawn with a plasma osmolality of 305 mOsm/kg
The three units, and what the number cannot tell you
pmol/L = pg/mL × 0.922314
derived from a molecular weight of 1,084.23 Da for the nonapeptide arginine vasopressin
- pg/mL = ng/L
- a picogram per millilitre and a nanogram per litre are the same concentration. North American reports usually print pg/mL and much of Europe prints pmol/L, so this is a conversion readers genuinely need
- × 0.922314
- the molar factor, from the mass of arginine vasopressin, 1,084.23 daltons. The factor is close to one, which makes the two scales easy to confuse: 4 pg/mL and 4 pmol/L differ by only 8%, so a figure quoted without its unit is often assumed to be either
- the number is half a measurement
- AVP is released in response to plasma osmolality above a threshold of roughly 280–285 mOsm/kg, and thereafter rises steeply — of the order of 0.4 pg/mL for each 1 mOsm/kg, in Robertson’s original work. Any AVP result is therefore interpreted as a pair with a simultaneous plasma osmolality, never against a range alone
- why copeptin is measured instead
- copeptin is the 39-residue C-terminal glycopeptide of the same precursor, pro-vasopressin, and is released in equimolar amounts with AVP. It is stable at room temperature for days, needs no special handling, and is measured on a routine automated platform — so it reports AVP secretion without AVP’s pre-analytical problems
- platelet-bound hormone
- a substantial fraction of circulating AVP is carried by platelets rather than free in plasma. That makes the measured plasma concentration depend on how the specimen was collected and separated as much as on how much hormone the pituitary released
Worked example
AVP 2.5 pg/mL, drawn with a plasma osmolality of 305 mOsm/kg
2.5 pg/mL = 2.50 ng/L — the same number in the other mass convention
2.5 × 0.922314 = 2.31 pmol/L, which is how most European laboratories would report it
Against the quoted interval, 0.0–4.7 pg/mL (0.00–4.33 pmol/L), 2.5 pg/mL is inside the range and the report will not flag it
That is exactly the trap. At a plasma osmolality of 305 mOsm/kg — some 20 mOsm/kg above the osmotic threshold — AVP should be several times this, and urine should be maximally concentrated. An AVP of 2.5 pg/mL with dilute urine at that osmolality is inappropriately low, and points to partial cranial diabetes insipidus
The same 2.5 pg/mL drawn at a plasma osmolality of 285 mOsm/kg would be entirely appropriate. The unit conversion is exact; the interpretation depends on a second number this page does not convert
Why AVP is rarely measured, and what is measured instead
| Problem with measuring AVP | Consequence | How copeptin avoids it |
|---|---|---|
| Degraded rapidly by plasma peptidases ex vivo | The result falls unless the sample is chilled, spun cold and frozen within about an hour | Stable at room temperature for days and at 4 °C for longer |
| Most of the circulating hormone is platelet-bound | The plasma concentration depends on collection and separation technique, not only on secretion | Measured in plasma or serum without a platelet-associated fraction to lose |
| Very low circulating concentrations, in the low pg/mL range | Assays are near their detection limit exactly where the clinical question lies — is AVP low or absent? | Circulates at nanomolar concentrations, comfortably within an automated assay’s range |
| Radioimmunoassay with extraction, sent away in batches | Days to weeks for a result, so it cannot inform a water deprivation test in real time | Routine automated immunoassay, same-day result |
| Released in equimolar amounts with copeptin | — | This is the point: copeptin is a stoichiometric surrogate for AVP secretion, not an approximation of it |
The pattern the water deprivation test is looking for
| Diagnosis | Plasma osmolality after deprivation | Urine osmolality | AVP or copeptin | Response to desmopressin |
|---|---|---|---|---|
| Cranial (central) diabetes insipidus — AVP deficiency | High | Remains dilute | Inappropriately low | Urine concentrates |
| Nephrogenic diabetes insipidus — AVP resistance | High | Remains dilute | High | No concentration |
| Primary polydipsia | Normal or low | Concentrates, often incompletely | Appropriate for osmolality | Not usually required |
| SIAD (hyponatraemia, not polyuria) | Low | Inappropriately concentrated | Detectable or high despite low osmolality | Not applicable |
The right hormone and the wrong analyte
Arginine vasopressin is the posterior pituitary hormone that defends plasma osmolality. Released when osmoreceptors detect a plasma osmolality above a threshold of roughly 280 to 285 mOsm/kg, it acts on V2 receptors in the renal collecting duct to insert aquaporin-2 channels and reabsorb water. Above that threshold the relationship is steep and close to linear — in Robertson’s original radioimmunoassay work, of the order of 0.4 pg/mL for each additional milliosmole per kilogram — which is why an AVP result is interpreted as one half of a pair with a simultaneous plasma osmolality and means very little against a reference interval alone.
The reason the hormone is so rarely measured is not that it is unimportant but that it is a bad analyte. AVP is extremely unstable once the blood is out of the patient: plasma peptidases degrade it within the hour unless the specimen is chilled immediately, centrifuged cold and the plasma frozen, and a large part of what circulates is bound to platelets rather than free in plasma, so the measured concentration depends on how the sample was collected and separated as much as on what the pituitary did. On top of that, the concentrations involved sit in the low picograms per millilitre, right at the detection limit of the extraction radioimmunoassays used to measure them, exactly where the clinical question — is AVP low or simply absent? — needs the most precision. A low result is therefore more often a mishandled tube than a failing pituitary.
Copeptin has largely replaced it, and the substitution is worth stating plainly. Copeptin is the 39-residue C-terminal glycopeptide of pro-vasopressin, cleaved from the same precursor and secreted in equimolar amounts with the hormone itself. It is stable at room temperature for days, requires no special handling, circulates at concentrations an automated immunoassay handles comfortably, and can be reported the same day. It is not an approximation of AVP secretion; it is a stoichiometric marker of it. Hypertonic saline-stimulated and arginine-stimulated copeptin protocols now discriminate AVP deficiency from primary polydipsia better than the indirect water deprivation test, which relied on urine concentrating ability rather than on measuring the hormone at all.
Where AVP or copeptin is measured, the diagnostic context is almost always polyuria and polydipsia and the question is a three-way one: cranial diabetes insipidus, now better called AVP deficiency, in which the hormone is not secreted; nephrogenic diabetes insipidus, or AVP resistance, in which it is secreted but the kidney cannot respond; and primary polydipsia, in which drinking rather than hormone failure drives the urine output. A water deprivation test separates them by watching plasma and urine osmolality diverge and then giving desmopressin. The hormone measurement, when it is available, tells you which side of that divergence the defect sits on. The units are the simple part: picograms per millilitre and nanograms per litre are the same number, and picomoles per litre is that number multiplied by 0.922314 — close enough to one that a figure quoted without its unit is easy to misread.
Frequently asked questions
How do I convert vasopressin from pg/mL to pmol/L?
Multiply by 0.922314, from a molecular weight of 1,084.23 daltons for the nonapeptide. An AVP of 2.5 pg/mL is 2.31 pmol/L. Picograms per millilitre and nanograms per litre are the same number, and because the molar factor is so close to one, a value quoted without its unit is easily mistaken for the other scale.
Why is vasopressin so rarely measured?
Because it is extremely unstable ex vivo. Plasma peptidases degrade it within about an hour unless the specimen is chilled immediately, centrifuged cold and frozen, and most of the circulating hormone is platelet-bound, so the plasma result reflects collection technique as much as secretion. Add concentrations at the detection limit of the assay and a send-away turnaround, and a low result is more often the specimen than the patient.
What is copeptin, and why has it replaced ADH measurement?
Copeptin is the C-terminal glycopeptide fragment of pro-vasopressin, cleaved from the same precursor and released in equimolar amounts with AVP. It is stable at room temperature, needs no special handling, circulates at concentrations an automated assay measures easily and can be reported the same day — so it reports AVP secretion without AVP’s pre-analytical fragility.
What is a normal ADH level?
One named assay quotes 0.0–4.7 pg/mL (Labcorp test 046557), but a value inside that range proves nothing on its own. AVP secretion is driven by plasma osmolality, so the result is only interpretable against a simultaneous osmolality: 2.5 pg/mL is appropriate at 285 mOsm/kg and inappropriately low at 305 mOsm/kg with dilute urine.
How does vasopressin separate cranial from nephrogenic diabetes insipidus?
By whether the hormone is present when it should be. After water deprivation raises plasma osmolality, urine stays dilute in both, but AVP or copeptin is inappropriately low in cranial diabetes insipidus (AVP deficiency) and high in nephrogenic diabetes insipidus (AVP resistance). Desmopressin then concentrates the urine in the first and not in the second.
Related calculators
References
- Fenske W, Refardt J, Chifu I, et al. A copeptin-based approach in the diagnosis of diabetes insipidus. N Engl J Med. 2018;379(5):428–439.
- Christ-Crain M, Fenske W. Copeptin in the diagnosis of vasopressin-dependent disorders of fluid homeostasis. Nat Rev Endocrinol. 2016;12(3):168–176.
- Robertson GL, Mahr EA, Athar S, Sinha T. Development and clinical application of a new method for the radioimmunoassay of arginine vasopressin in human plasma. J Clin Invest. 1973;52(9):2340–2352.
- Labcorp. Test 046557: Antidiuretic Hormone (ADH) Profile — reference interval 0.0–4.7 pg/mL; plasma to be separated in a refrigerated centrifuge and frozen immediately; ADH unstable at room temperature and refrigerated. Accessed 2026.
- Winzeler B, Cesana-Nigro N, Refardt J, et al. Arginine-stimulated copeptin measurements in the differential diagnosis of diabetes insipidus: a prospective diagnostic study. Lancet. 2019;394(10198):587–595.
Medical Disclaimer: The tools and content provided here are for educational and reference purposes only. They are not intended to substitute for professional medical advice, diagnosis, or treatment. Clinical decisions should always be based on the comprehensive assessment of a qualified healthcare professional.