BNP Unit Converter
BNP Unit Converter
Convert BNP between pg/mL, ng/L and pmol/L, and see why BNP and NT-proBNP are different molecules that cannot be read against each other's thresholds.
BNP converter
Mass ⇄ molarBNP 320 pg/mL
Formula and conversion factor
pg/mL = pmol/L ÷ 0.2887
- 0.2887
- derived from the molecular weight of BNP-32, the biologically active peptide, 3464 Da
- ng/L
- numerically identical to pg/mL
- NT-proBNP
- a different molecule with its own reference ranges — not interchangeable with BNP despite the shared name
Worked example
BNP 320 pg/mL
320 × 0.2887 = 92.4 pmol/L
= 320 ng/L, numerically identical to pg/mL
Rule-out thresholds and confounders
| Factor | Effect |
|---|---|
| Non-acute setting | Heart failure unlikely below 35 pg/mL |
| Acute breathlessness | Heart failure unlikely below 100 pg/mL |
| Age, atrial fibrillation, renal impairment, female sex | Raise BNP independent of cardiac function |
| Obesity | Lowers BNP — a normal result does not exclude heart failure |
| Sacubitril/valsartan | Raises BNP via neprilysin inhibition — trend NT-proBNP instead |
What BNP measures, and where it is misread
B-type natriuretic peptide is secreted by ventricular myocytes in response to wall stress, and its main clinical role is ruling heart failure in or out in a patient presenting with breathlessness. The distinction between pg/mL and ng/L is trivial — they are numerically identical — but the distinction between BNP and NT-proBNP is not, and the two names are used interchangeably far too often. They are different molecules, cleared by different routes, with different reference ranges, and a BNP result cannot be read against an NT-proBNP threshold or the reverse.
Interpretation depends heavily on context. In the non-acute setting a BNP below 35 pg/mL makes heart failure unlikely; in acute breathlessness the rule-out threshold rises to 100 pg/mL, because acute haemodynamic stress raises the baseline. Levels also rise with age, atrial fibrillation and renal impairment independent of cardiac function, and — in the other direction — are lowered by obesity, so a normal result in a very obese patient does not exclude heart failure and should be interpreted cautiously alongside the rest of the clinical picture.
Treatment with sacubitril/valsartan complicates BNP specifically. The drug inhibits neprilysin, the enzyme that normally degrades BNP, so BNP rises on treatment even as the patient improves, while NT-proBNP — which is not a neprilysin substrate — continues to fall. In any patient established on sacubitril/valsartan, NT-proBNP is the marker to trend; a rising BNP in that context reflects the drug, not worsening disease.
Frequently asked questions
How do I convert BNP from pg/mL to pmol/L?
Multiply by 0.2887. A BNP of 320 pg/mL is 92.4 pmol/L. pg/mL and ng/L are numerically identical, so no conversion is needed between those two.
Is BNP the same as NT-proBNP?
No. They are different molecules — BNP is the active hormone, NT-proBNP the inactive fragment cleaved alongside it — with different clearance routes and different reference ranges. Results are not interchangeable between the two.
Why might BNP be normal in a patient with heart failure?
Obesity lowers BNP independent of cardiac status, so a normal result in a markedly obese patient does not exclude heart failure. The rule-out threshold also depends on whether the presentation is acute or non-acute.
Why does BNP rise on sacubitril/valsartan?
The drug inhibits neprilysin, the enzyme that degrades BNP, so BNP rises on treatment even as heart failure improves. NT-proBNP is not affected and should be used to monitor these patients instead.
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References
- McDonagh TA et al. 2021 ESC Guidelines for the diagnosis and treatment of acute and chronic heart failure. Eur Heart J. 2021;42(36):3599–3726.
- Mueller C et al. Heart Failure Association of the ESC practical guidance on the use of natriuretic peptide concentrations. Eur J Heart Fail. 2019;21(6):715–31.
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.