Prealbumin (Transthyretin) Unit Converter
Prealbumin (Transthyretin) Unit Converter
Convert prealbumin between mg/dL, mg/L and µmol/L — and know two things about it: despite the name it has nothing to do with albumin, and it falls in inflammation independently of nutrition, which is why ASPEN no longer recommend it as a nutrition marker.
Prealbumin (Transthyretin) converter
Mass ⇄ molarPrealbumin 25 mg/dL in a well outpatient, then 9 mg/dL with a CRP of 180 mg/L on day 4 of sepsis
The conversion, and the molecular weight behind it
µmol/L = mg/dL × 0.181884
because 0.181884 = 1 mg/dL (10⁻² g/L) ÷ 54,980 g/mol, the molecular weight of the transthyretin tetramer
- MW 54,980
- transthyretin circulates as a homotetramer of four 127-residue subunits of about 13.7 kDa each. The molar factor is derived from the tetramer, which is the circulating form the assay measures
- mg/dL → mg/L is × 10
- so a prealbumin of 25 mg/dL is 250 mg/L. Both are in use; mg/dL is the commoner clinical report and mg/L appears on some European ones
- µmol/L
- 25 mg/dL is 4.55 µmol/L. Molar reporting is less common for this analyte than for most, but it does appear, and a single-figure result in the low single digits is almost certainly µmol/L rather than mg/dL
- prealbumin has nothing to do with albumin
- the name is an accident of paper electrophoresis — the protein runs ahead of albumin, so it was called prealbumin. It is a structurally unrelated protein with a different function, which is why the preferred name is now transthyretin: it transports thyroxine and, with retinol-binding protein, vitamin A
- the half-life is the point
- about two days, against roughly twenty for albumin. That is the whole reason prealbumin was adopted as a nutritional marker — it responds within days rather than weeks — and it is also why it drops so quickly in acute inflammation
Worked example
Prealbumin 25 mg/dL in a well outpatient, then 9 mg/dL with a CRP of 180 mg/L on day 4 of sepsis
25 mg/dL = 250 mg/L = 4.55 µmol/L (25 × 0.181884 = 4.5471)
25 mg/dL sits mid-interval against Mayo's adult 19–38 mg/dL, and in a well patient that is unremarkable
Now the same patient on day 4 of a severe pneumonia: prealbumin 9 mg/dL (90 mg/L, 1.64 µmol/L) with a CRP of 180 mg/L. That is inflammation, not malnutrition. Interleukin-6-driven reprioritisation of hepatic synthesis cuts transthyretin production while the acute-phase proteins rise, whatever the patient is being fed
Which is why the fall says nothing useful about feeding. Giving more protein and energy will not correct it while the CRP is high, and a rise as the CRP falls reflects resolving inflammation rather than nutritional repletion
The half-life is what makes both directions fast: about two days for transthyretin against roughly twenty for albumin, so prealbumin moves within a few days where albumin takes weeks
Two things the name gets wrong
| Assumption | Reality |
|---|---|
| “Prealbumin is a form of albumin, or related to it” | It is not. The name comes from paper electrophoresis, where the protein migrates ahead of the albumin band. It is a structurally unrelated 55 kDa homotetramer with a completely different function, and its preferred name is transthyretin — it transports thyroxine, and vitamin A in complex with retinol-binding protein. It is also the protein that misfolds in hereditary and wild-type transthyretin amyloidosis |
| “A low prealbumin means the patient is malnourished” | Not on its own. Transthyretin is a negative acute-phase reactant: hepatic synthesis is reprioritised away from it in inflammation, so it falls in sepsis, trauma, surgery and any inflammatory illness regardless of intake. It also falls in liver disease, because the liver makes it, and in protein-losing states. A low prealbumin with a raised CRP indicates inflammation |
| “A normal or rising prealbumin means feeding is working” | Not reliably. A rise as inflammation resolves tracks the falling CRP rather than nutritional repletion, and a normal value in an inflamed patient is not reassurance about intake |
| “A high prealbumin is good nutrition” | No. It is seen with corticosteroids, with high-dose NSAIDs and in chronic kidney disease — particularly on dialysis, where reduced renal catabolism raises it — and means nothing nutritional |
What ASPEN say, and what to use instead
| Point | Position |
|---|---|
| Should albumin or prealbumin be used as nutrition markers? | No. The 2021 ASPEN position paper concludes that these proteins “do not serve as proxy measures of total body protein or total muscle mass and should not be used as nutrition markers” |
| What do they actually reflect? | Inflammation. ASPEN state that serum concentrations of albumin and prealbumin “decline in the presence of inflammation, regardless of underlying nutrition status”, and should be recognised as inflammatory markers associated with nutrition risk |
| What establishes malnutrition instead? | A nutrition-focused assessment: dietary intake history, weight loss over time, physical examination for loss of muscle mass and subcutaneous fat, fluid accumulation, and reduced functional capacity such as grip strength — the domains used by the GLIM and ASPEN/Academy criteria |
| Does prealbumin retain any role? | As a marker of the inflammatory state and of nutrition risk, and historically in monitoring response to nutrition support in patients who are not inflamed — but not as the measurement on which a diagnosis of malnutrition rests. Interpreted alongside CRP, a low prealbumin with a high CRP is an inflammation finding |
| What should be measured with it? | CRP, on the same sample. Without it a low prealbumin cannot be interpreted at all |
Not albumin, and not a nutrition marker
Prealbumin is reported in milligrams per decilitre, milligrams per litre or micromoles per litre. Milligrams per litre are ten times the mg/dL figure, so 25 mg/dL is 250 mg/L, and the molar conversion comes from transthyretin’s tetramer molecular weight of 54,980: one milligram per decilitre is 0.181884 micromoles per litre, so 25 mg/dL is 4.55 µmol/L. The protein circulates as a homotetramer of four identical subunits, which is the form the assay measures and the form the molar factor is derived from.
The first thing to know is that the name is misleading. Prealbumin has nothing to do with albumin. It is called prealbumin only because it migrates ahead of the albumin band on paper electrophoresis; structurally and functionally it is an unrelated protein, and its proper name is transthyretin — it transports thyroxine, and vitamin A in complex with retinol-binding protein. It is also the protein that misfolds in hereditary and wild-type transthyretin amyloidosis. Confusing it with albumin, or assuming the two behave as a pair, is the commonest misreading of the result.
The second thing is what the measurement actually responds to. Transthyretin has a half-life of about two days, against roughly twenty for albumin, and that short half-life is precisely why it was adopted as a nutritional marker: it moves within days rather than weeks, so it looked like a way of watching nutrition support work. But it falls in inflammation independently of nutrition. It is a negative acute-phase reactant — interleukin-6-driven reprioritisation of hepatic protein synthesis diverts the liver towards the acute-phase proteins and away from transthyretin — so it drops in sepsis, trauma, surgery and any inflammatory illness whatever the patient is being fed. It also falls in liver disease, because the liver makes it, and in protein-losing states. The practical rule that follows is short: a low prealbumin with a raised CRP says inflammation, not malnutrition, and a prealbumin measured without a CRP cannot be interpreted at all.
This is now formal guidance rather than a caveat. ASPEN’s 2021 position paper on visceral proteins concludes that albumin and prealbumin “do not serve as proxy measures of total body protein or total muscle mass and should not be used as nutrition markers”, and that their concentrations “decline in the presence of inflammation, regardless of underlying nutrition status” — they should be understood as inflammatory markers associated with nutrition risk. Malnutrition is established instead by assessment: dietary intake history, weight change over time, physical examination for loss of muscle and subcutaneous fat, fluid accumulation and reduced functional capacity such as grip strength. A rising prealbumin during nutrition support most often reflects resolving inflammation rather than repletion, and a high value means little — corticosteroids, high-dose non-steroidal anti-inflammatories and chronic kidney disease, particularly on dialysis, all raise it.
Frequently asked questions
How do you convert prealbumin from mg/dL to µmol/L?
Multiply by 0.181884, which is one milligram per decilitre divided by transthyretin’s tetramer molecular weight of 54,980 g/mol. A prealbumin of 25 mg/dL is 4.55 µmol/L, and 250 mg/L — ten times the mg/dL figure — is the same concentration again. Divide by 0.181884 to go the other way.
Is prealbumin related to albumin?
No, despite the name. Prealbumin was named only because it migrates ahead of albumin on paper electrophoresis; it is a structurally unrelated 55 kDa homotetramer whose proper name is transthyretin, and it transports thyroxine and, with retinol-binding protein, vitamin A. It is also the protein that misfolds in transthyretin amyloidosis. The two proteins share a serum electrophoretogram and nothing else.
Does a low prealbumin mean malnutrition?
Not on its own, and usually not in an unwell patient. Transthyretin is a negative acute-phase reactant: inflammation reprioritises hepatic synthesis away from it, so it falls in sepsis, trauma, surgery and any inflammatory illness regardless of what the patient is being fed. It also falls in liver disease and in protein-losing states. A low prealbumin alongside a raised CRP indicates inflammation, not a protein-energy deficit, which is why a CRP should be measured on the same sample.
Why was prealbumin used as a nutritional marker at all?
Because of its half-life — about two days, against roughly twenty for albumin. That made it look like a way to watch nutrition support take effect within days rather than weeks, where albumin moves far too slowly to be useful. The problem is that the same short half-life makes it drop sharply and quickly in inflammation, so what it tracks in a sick patient is the inflammatory state rather than the diet.
Do guidelines still recommend prealbumin for nutritional assessment?
No. ASPEN’s 2021 position paper on visceral proteins concludes that albumin and prealbumin should not be used as nutrition markers, because they do not act as proxies for total body protein or muscle mass and decline in inflammation regardless of nutritional status; they are better understood as inflammatory markers associated with nutrition risk. Malnutrition is established by assessment instead — intake history, weight change, loss of muscle and fat stores, and functional measures such as grip strength.
Related calculators
References
- Mayo Clinic Laboratories. Test ID: PALB — Prealbumin, Serum. Nephelometry. Reference values: >18 years 19–38 mg/dL; ≤18 years 12–32 mg/dL. Half-life approximately 2 days.
- Evans DC, Corkins MR, Malone A, et al. The use of visceral proteins as nutrition markers: an ASPEN position paper. Nutr Clin Pract. 2021;36(1):22–28. doi:10.1002/ncp.10588 — albumin and prealbumin “do not serve as proxy measures of total body protein or total muscle mass and should not be used as nutrition markers”.
- Cederholm T, Jensen GL, Correia MITD, et al. GLIM criteria for the diagnosis of malnutrition — a consensus report from the global clinical nutrition community. Clin Nutr. 2019;38(1):1–9.
- UniProt P02766 (TTHY_HUMAN), transthyretin — circulating homotetramer, molecular weight 54,980 used for the molar conversion on this page.
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.