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Natriuretic peptide

StatusLab measurement

PeptideHound Staff · Last editorially reviewed · 27 sources

For most people who look it up, a natriuretic peptide is a hormone the heart puts into the blood when the muscle is under strain, met as a name on a laboratory report. A 2018 review calls B-type natriuretic peptide and the N-terminal fragment of its prohormone well-established biomarkers for patients with heart failure.

A biomarker is a figure read off a blood sample, and this one stands in for strain on heart muscle. Two real groups show the scale. Among 519 women without known heart disease, the median N-terminal figure was 68.8 ng/l. Among 4,822 patients in the PARAGON-HF heart failure trial, the median was 911 pg/mL. One nanogram per litre is one picogram per millilitre, so those medians sit on one scale about thirteen-fold apart. That gap is the whole test: strained hearts read higher.

The figure steers real decisions, and it also decides who gets into a trial. SPIRRIT-HFpEF enrols above 300 ng/L in sinus rhythm, or above 750 ng/L in atrial fibrillation, with an adjustment for elevated body mass index. Read that carefully. Those are entry rules for one study rather than a diagnostic line, and a trial needing two thresholds for two heart rhythms plus a correction for body size is telling you the figure is never read alone. The same 2018 review says cutoff levels, and the effects of renal function and age, should be reassessed.

Two hospital medicines come from this family, and they are a separate matter from the test. Nesiritide, recombinant human B-type natriuretic peptide, was approved in the US in 2001 as a drip for acutely decompensated heart failure, and in a 2011 trial of 7141 patients it did not change death or readmission at 30 days while raising rates of low blood pressure. Carperitide, an A-type natriuretic peptide drip, is used primarily in Japan. Neither record says anything about what a figure on a laboratory slip means.

Evidence: a blood marker in established clinical use · readings are shifted by kidney function, age, body size and heart rhythm · evidence for guiding day-to-day management is mixed · the hospital drug form, nesiritide, was tested in a 7141-patient trial

What is a natriuretic peptide, and why is it in a blood test?

human RCT

The heart is not only a pump: under mechanical strain it also behaves like a gland, releasing hormones that a laboratory can measure. A myocyte is a heart muscle cell, and that is where these particular hormones are manufactured. Investigators who measured 519 women without known cardiovascular disease described B-type natriuretic peptide as a marker of myocyte stress.2 A 2018 review in Postgrad Med calls it and the fragment of its prohormone well-established biomarkers for patients with heart failure.1 A biomarker is a figure read off a blood sample that stands in for something harder to observe directly. Animal work agrees: a 2026 experiment on heart muscle cells and a heart failure animal model treated these hormones as pathological markers of cardiac stress.8

What is the difference between BNP, NT-proBNP and pro-BNP?

review

Three names appear on laboratory reports, and they are not three separate measurements. A prohormone is the longer molecule that a hormone is cut out of. The 2018 review describes the pair as B-type NP (BNP) and the N-terminal fragment of its prohormone (NT-proBNP), which is where pro-brain natriuretic peptide originates as a search term.1 The heart manufactures the long form, cleaves it, and both halves circulate. A laboratory measuring one half will not report the same figure as a laboratory measuring the other. Neprilysin is the enzyme responsible for clearing BNP, and one established class of heart failure medicine inhibits it. The same review records the prevention of BNP degradation by angiotensin receptor/neprilysin inhibitors (ARNIs), and may present a challenge in the interpretation of levels of BNP.1

What is a natriuretic peptide test used for?

review

Two jobs, mainly, and the 2018 review names both: these biomarkers have consistently demonstrated their value in the diagnosis and prognostication of HF, where HF is heart failure.1 Diagnosis means establishing whether heart failure is what is going on, and prognostication is the field's word for what is likely to happen next. A 2014 Indian consensus document puts the job more fully, writing that biomarkers act as indicators for the presence, degree of severity and prognosis of the disease, they may be employed in combination with the present conventional clinical assessments.9 That final clause is the part readers skip: in combination with an examination, not instead of one. A 2017 review is blunt about a third job people assume it does. Biomarkers have revolutionized the diagnosis of heart failure (HF), but it remains unclear how to use biomarkers to guide management of HF.10

What does a high B-type natriuretic peptide mean?

human RCT

A high figure indicates that heart muscle is under more mechanical strain than it should be. It does not indicate why, and on its own it does not identify a particular disease. The research behind this page describes it as a marker of myocyte stress, and heart failure is the condition it is most frequently deployed to investigate.2 Two populations illustrate the scale. Among 519 women without known heart disease, the median (Q1 to Q3) NT-proBNP of the cohort was 68.8 ng/l (40.3 to 127.3 ng/l), whereas among 4822 patients randomized in PARAGON-HF, a trial in heart failure with preserved ejection fraction, the equivalent median was 911 pg/mL.23 One nanogram per litre is one picogram per millilitre, so those medians occupy a single scale approximately thirteen-fold apart. Severity and causation are different questions, however, and a concentration addresses only the first.9

What does a low natriuretic peptide reading mean?

human RCT

A low figure indicates that heart muscle was not under much mechanical strain when the blood was drawn. Attaching a name to low is harder than it sounds, because the comparison population does the work. Among 519 women without known heart disease the middle half of the group ran from 40.3 to 127.3 ng/l, and those are observations in women without heart disease rather than a reference range any laboratory publishes.2 A 2026 review in Circulation exposes the gap from the opposite direction, arguing that recent trials might have reported larger effects had they permitted the participation of patients with class III obesity or with lower natriuretic peptide levels.11 Participants with lower concentrations were deliberately excluded.11 So a modest figure in somebody who already has symptoms rests on considerably thinner ground than a high one does.

Is there a normal range, or a single cut-off?

human RCT

Not one figure that travels everywhere, on the research behind this page. The 2018 review closes by saying cutoff levels and the effects of individual patient characteristics, such as renal function and age, on biomarker concentrations should be reassessed.1 That is the field conceding that its thresholds were still being argued over, and the trials demonstrate the same difficulty from inside. SPIRRIT-HFpEF sets entry at N-terminal pro-B-type natriuretic peptide >300 ng/L (in sinus rhythm) or >750 ng/L (in atrial fibrillation), with pre-specified adjustment for elevated body mass index.4 A single trial requires two thresholds for two heart rhythms, plus a correction for body size. Read that carefully: those are eligibility rules written for one study, and they are not a line anybody should measure themselves against. One bedside instrument carries a registered B-type Natriuretic Peptide (BNP) Method Comparison Evaluation.12

What moves a reading other than the heart?

human RCT

Several things, and this is the part a bare figure hides. The 2018 review names two outright, saying the effects of individual patient characteristics, such as renal function and age, on biomarker concentrations should be reassessed.1 Renal function describes how efficiently the kidneys clear the blood. Body size is the third. SPIRRIT-HFpEF applies a pre-specified adjustment for elevated body mass index to its entry threshold, which is a trial writing body size into its own eligibility rules, and a 2026 Circulation review describes recent large trials as showing general uniformity with respect to the presence of excess adiposity.411 Kidney disease is common alongside heart failure: in PARAGON-HF, chronic kidney disease (47%) were more prevalent than in previous trials of HFpEF.3 None of that makes a figure wrong. It means a figure is interpreted beside somebody's age, kidney function and build.

Why does atrial fibrillation change the number used?

human RCT

Atrial fibrillation is an irregular heart rhythm originating in the upper chambers, and it displaces the figure far enough that a trial will not apply one threshold to everybody. SPIRRIT-HFpEF sets entry at N-terminal pro-B-type natriuretic peptide >300 ng/L (in sinus rhythm) or >750 ng/L (in atrial fibrillation), sinus rhythm being the normal regular beat.4 That is two and a half times the concentration, for the same marker in the same trial, with the rhythm as the only variable that changed. Why the figure runs higher in atrial fibrillation is not answered by the research behind this page, and the trial writes the difference into its eligibility rules without explaining it. A 2016 paper on prediction of atrial fibrillation risk in the community works the adjacent question.13 What the entry rule demonstrates is plainer: a concentration interpreted without knowing the rhythm is interpreted without part of its context.

Is a natriuretic peptide the same as a troponin test?

human RCT

No, although a hospital panel will frequently carry both. A 2016 analysis of 519 women measured them alongside each other and set the difference out in a single line: cardiac troponin, a marker of myocyte injury, and B-type natriuretic peptide, a marker of myocyte stress.2 Injury means heart muscle cells have been damaged, which is what a heart attack does, whereas stress means the muscle is being stretched and worked against a load. A 2014 consensus document sorts blood markers by what they report on, listing biomarkers of myocyte necrosis, myocardial remodeling, neurohormonal activation, etc.9 Necrosis is tissue death, and remodelling is the architecture of the heart altering across months. Two figures on one sheet answer two different questions, and a high result on one says nothing about the other.

Can medicines change a natriuretic peptide figure?

systematic review

Yes, which is one reason a figure is read against whatever somebody already takes. In the UK HARP-III trial, 414 participants with an estimated glomerular filtration rate (GFR) 20 to 60 mL/min/1.73 m2 were assigned one of two blood pressure medicines.14 Glomerular filtration rate is a measure of kidney clearance. Against irbesartan, sacubitril/valsartan left N-terminal readings lower by 18% (95% CI, 11-25).14 A 2019 analysis pooled 132 patients for levosimendan and 125 patients for control groups, where levosimendan was associated with a significantly reduced BNP level.15 Not everything shifts it. In the LEAF-CHF study of chronic heart failure, febuxostat did not reduce plasma BNP levels at week 24 in patients with CHF.16 A figure that falls once a medicine starts is a figure answering a medicine, which is not the same as a heart that has mended.

How is the sample taken, and can it be read at the bedside?

systematic review

From an ordinary blood draw, and sometimes from a machine in the clinic rather than a central laboratory. A point-of-care test is one run where the patient already is, with a figure back in minutes. A 2018 systematic review searched four databases and found nine papers describing data from seven studies, on the clinical diagnostic accuracy of POCT in a total of 2277 primary care patients with acute cardiopulmonary symptoms.17 POCT is that bedside kind of test, and one of the seven covered B-type natriuretic peptide (BNP) in heart failure.17 The verdict was careful: there is currently limited and inconclusive evidence that actual GP use of POCT leads to more accurate diagnosis and affects clinical management.17 What those papers put in doubt is not the marker. It is how much a faster figure changes what anybody does next.

Is the reading used outside heart failure?

human pilot / early trial

Yes, in several places, and the ground is thinner there than under heart failure. In cancer care, a 2019 review says troponins and natriuretic peptides are the most commonly used biomarkers, then adds that high-quality evidence supporting their use is lacking.18 A 2020 paper in JACC CardioOncology covers cardiac biomarkers during cancer therapy.19 Around heart surgery, a 2021 article weighed the modest incremental benefit of N-terminal pro brain natriuretic peptide levels when added to almost 20 other variables, for the preoperative prediction of AKI after cardiac surgery.20 AKI is acute kidney injury. The same article says there are important additional questions still to be answered before this biomarker might be used for this purpose.20 A 2007 paper from China asks the same of children, under the title value of B-type natriuretic peptide in congenital heart disease.21 Commonly used is not the same as settled.

Does the reading say what happens next?

human pilot / early trial

Partly. The limits are worth stating plainly. The 2018 review says these biomarkers have consistently demonstrated their value in the diagnosis and prognostication of HF, and the 2014 consensus document places the marker among indicators of prognosis of the disease.19 Then the qualifications arrive. The same 2018 review says their ability to help clinicians in making treatment decisions remains debated.1 A 2013 study of people having planned stent procedures reported that post-interventional cardiac biomarker release has lower prognostic relevance compared with standard risk markers in patients with stable coronary artery disease.22 A 2017 review concluded that the current data on using biomarkers to guide HF management remain mixed.10 Prognosis is a statement about what happens across a group of people. It does not tell one person what will happen to them.

Is a natriuretic peptide ever given as a medicine?

systematic review

Yes, as a hospital drip, and that is a different subject from the blood test. Nesiritide is the recombinant form of human B-type natriuretic peptide, made by engineered cells, and its amino acid sequence is identical to that of endogenous human BNP.2324 Endogenous means made by the body itself. Sold as Natrecor, it is given into a vein in hospital.25 It was approved and launched in the US in August 2001 for patients with acute heart failure who are short of breath at rest or at minimal activity.7 Then its standing fell. The ASCEND-HF trial randomised 7141 patients, and nesiritide did not change the rate of death and readmission.6 Its authors said it cannot be recommended for routine use in the broad population of patients with acute heart failure.6 Carperitide, an A-type natriuretic peptide, is given by vein for acute heart failure, mainly in Japan.5 A 2025 analysis of nine studies says its clinical effectiveness has not been established.5 Harms are covered on the Natriuretic peptide safety page, trial results are weighed on the Natriuretic peptide benefits page, and the rates the trials used are listed on the Natriuretic peptide dosage page.

What does the hormone itself do?

animal model

The measuring came after the biology, and most of that biology sits in animals. In a 2026 experiment on heart muscle cells and a heart failure animal model, idebenone cut expression of atrial natriuretic peptide (ANP) and brain natriuretic peptide (BNP) in cardiomyocytes.8 A 2001 experiment in salt-sensitive rats read gene activity rather than blood level, and LV atrial natriuretic peptide mRNA upregulation in DS rats was suppressed by two blood pressure medicines given together.26 Upregulation means the gene was read harder, so the heart was building more of the hormone. In rats that developed chronic heart failure after coronary artery ligation, finerenone reduced plasma prohormone of brain natriuretic peptide levels.27 Animal work describes what the hormone does. It does not tell a person what their own figure means.

What does a single reading not establish?

human pilot / early trial

A single figure is one measurement, taken at one moment, by one method, in one body with its own age, kidney function and build. It counts mechanical strain on heart muscle; it is not a diagnosis, it does not establish a cause, and it does not settle what comes next for the person holding it. The reviews behind this page are explicit about the edges. The 2018 review says cutoff levels should be reassessed, and that the ability of these markers to help clinicians in making treatment decisions remains debated.1 The 2021 surgical article says there are important additional questions still to be answered before this biomarker might be used for this purpose.20 None of that makes the measurement unreliable, and none of it is a reason to dismiss a result. It means a figure is one input a clinician interprets alongside an examination, a history and the other investigations.

Regulatory status

A laboratory measurement for most readers · nesiritide, recombinant B-type natriuretic peptide, was approved in the US in 2001 as a hospital drip for acutely decompensated heart failure · carperitide, an A-type natriuretic peptide drip, is used primarily in Japan · a 2018 review says cutoff levels should be reassessed

What we don’t know

The gaps in the evidence matter as much as the findings.

  1. 01Where the line sits for one person. No source among the research behind this page gives a diagnostic cut-off, and a 2018 review says cutoff levels and the effects of individual patient characteristics should be reassessed.
  2. 02How far age, kidney function or body size shift a figure. The reviews behind this page name all three as influences, and none of them puts a number on the correction.
  3. 03Why atrial fibrillation needs a higher threshold. One trial writes 750 ng/L for atrial fibrillation against 300 ng/L in sinus rhythm, and no study among the research behind this page explains the gap.
  4. 04What a figure costs, or how quickly it comes back in ordinary care. No source among the research behind this page reports a price or a turnaround time.
  5. 05Whether acting on the figure changes what happens to people. A 2017 review found the data on using biomarkers to guide heart failure management mixed, and the question has stayed open since.
  6. 06How the different laboratory methods compare in daily use. One method comparison study is on the public trials register among the research behind this page, and no result from it appears in these sources.
  7. 07What a figure means in a child. A 2007 paper on the value of B-type natriuretic peptide in congenital heart disease sits among the research behind this page, and no figures from it are reported in these sources.
  8. 08Why giving a natriuretic peptide has not matched what measuring one suggests. Nesiritide did not change death or readmission in a 7141-patient trial, a 2025 analysis reports that carperitide's clinical effectiveness has not been established, and neither settles the reason.

Sources

  1. 1Utility of natriuretic peptides to assess and manage patients with heart failure receiving angiotensin receptor blocker/neprilysin inhibitor therapy Postgrad Med 2018. doi:10.1080/00325481.2018.1440873review
  2. 2Impact of Modifiable Risk Factors on B-type Natriuretic Peptide and Cardiac Troponin T Concentrations Am J Cardiol 2016. doi:10.1016/j.amjcard.2015.10.054human RCT
  3. 3Baseline Characteristics of Patients With Heart Failure and Preserved Ejection Fraction in the PARAGON-HF Trial Circ Heart Fail 2018. doi:10.1161/CIRCHEARTFAILURE.118.004962human RCT
  4. 4The Spironolactone Initiation Registry Randomized Interventional Trial in Heart Failure with Preserved Ejection Fraction (SPIRRIT-HFpEF): Rationale and design Eur J Heart Fail 2024. doi:10.1002/ejhf.3453human RCT
  5. 5Effect of carperitide on clinical outcomes among patients with acute heart failure: a meta-analysis of randomized and propensity‑matched studies BMC Cardiovasc Disord 2025. doi:10.1186/s12872-025-05394-0systematic review
  6. 6Effect of nesiritide in patients with acute decompensated heart failure N Engl J Med 2011. doi:10.1056/NEJMoa1100171human RCT
  7. 7Nesiritide (Scios) IDrugs 2002. PMID 12802704human pilot / early trial
  8. 8Idebenone protects against doxorubicin-induced cardiac injury by inhibiting ferroptosis in cardiomyocytes Exp Gerontol 2026. doi:10.1016/j.exger.2026.113039animal model
  9. 9The Indian Consensus Document on cardiac biomarker Indian Heart J 2014. doi:10.1016/j.ihj.2013.12.053review
  10. 10Using biomarkers to guide heart failure management Expert Rev Cardiovasc Ther 2017. doi:10.1080/14779072.2017.1366312review
  11. 11Does Characterization of Phenotypic Heterogeneity Provide Mechanistic Insights or Influence the Response to Treatment? Experience in Positive and Neutral Trials in Patients With Heart Failure and a Preserved Ejection Fraction Circulation 2026. doi:10.1161/CIRCULATIONAHA.126.079235review
  12. 12Alere Triage fs B-type Natriuretic Peptide (BNP) Method Comparison Evaluation NCT01434433registered trial
  13. 13Prediction of atrial fibrillation risk in the community Int J Cardiol 2016. doi:10.1016/j.ijcard.2016.01.115primary research
  14. 14Effects of Sacubitril/Valsartan Versus Irbesartan in Patients With Chronic Kidney Disease Circulation 2018. doi:10.1161/CIRCULATIONAHA.118.034818human RCT
  15. 15Effect of levosimendan in patients with acute decompensated heart failure : A meta-analysis Herz 2019. doi:10.1007/s00059-018-4693-3systematic review
  16. 16Efficacy and safety of the urate-lowering agent febuxostat in chronic heart failure patients with hyperuricemia: results from the LEAF-CHF study Heart Vessels 2025. doi:10.1007/s00380-024-02448-9human RCT
  17. 17Point-of-care testing in primary care patients with acute cardiopulmonary symptoms: a systematic review Fam Pract 2018. doi:10.1093/fampra/cmx066systematic review
  18. 18Role of Cardiovascular Biomarkers in the Risk Stratification, Monitoring, and Management of Patients with Cancer Cardiol Clin 2019. doi:10.1016/j.ccl.2019.07.015review
  19. 19Cardiac Biomarkers During Cancer Therapy: Practical Applications for Cardio-Oncology JACC CardioOncol 2020. doi:10.1016/j.jaccao.2020.08.014review
  20. 20Predicting acute kidney injury after cardiac surgery: much work still to be done Br J Anaesth 2021. doi:10.1016/j.bja.2021.09.005human pilot / early trial
  21. 21[Value of B-type natriuretic peptide in congenital heart disease] Zhonghua Er Ke Za Zhi 2007. PMID 17880807review
  22. 22Post-interventional cardiac biomarker release has lower prognostic relevance compared with standard risk markers in patients with stable coronary artery disease undergoing elective percutaneous coronary interventions Int J Cardiol 2013. doi:10.1016/j.ijcard.2013.07.058human pilot / early trial
  23. 23Nesiritide: harmful or harmless? Pharmacotherapy 2006. doi:10.1592/phco.26.10.1465review
  24. 24Nesiritide: past, present, and future Minerva Cardioangiol 2005. PMID 16333235review
  25. 25Nesiritide: a review of its use in acute decompensated heart failure Drugs 2003. doi:10.2165/00003495-200363010-00004review
  26. 26Effects of combination of ACE inhibitor and angiotensin receptor blocker on cardiac remodeling, cardiac function, and survival in rat heart failure Circulation 2001. doi:10.1161/01.cir.103.1.148animal model
  27. 27Finerenone, a novel selective nonsteroidal mineralocorticoid receptor antagonist protects from rat cardiorenal injury J Cardiovasc Pharmacol 2014. doi:10.1097/FJC.0000000000000091animal model