Lipoprotein(a), mass (mg/dL)
A cholesterol-carrying particle like LDL with an extra protein attached. Your level is mostly set by your genes and stays fairly steady through life.
AI-verified against cited sources. Awaiting expert reviewAlso called Lp(a), Lp-aLOINC 10835-7
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What it is
Lipoprotein(a), or Lp(a), is a particle in your blood that looks like LDL but has an extra protein, apolipoprotein(a), attached to it. Your genes set most of your Lp(a) level, and it usually reaches its adult level by about age 5. Diet and exercise change it very little. This version of the test reports the weight of Lp(a) in milligrams per deciliter (mg/dL). Some labs report particle count in nmol/L instead, and the two cannot be converted exactly.
Why it matters
Higher Lp(a) is linked to a higher lifetime chance of heart attack, stroke and narrowing of the aortic valve. This link holds even when LDL cholesterol is low. Because the level is mostly inherited and rarely changes, several guidelines suggest checking it at least once in adulthood. A high result is a reason to look more closely at your other heart risk factors with your clinician. It is not a verdict on its own.
If it’s low
A low level is the usual finding and is generally not a concern. Some studies have linked very low levels to a higher chance of type 2 diabetes. Researchers are still studying this, and it does not usually call for any action.
Common causes
- Your genes. Most people have low levels, and variation in the LPA gene decides this
- Advanced liver disease, which can lower the amount your liver makes
- An overactive thyroid (hyperthyroidism)
- Severe acute illness such as sepsis or major burns, usually for a short time
What can help
- Nothing is usually needed for a low Lp(a)
- If you have other symptoms or conditions, ask your clinician whether the cause is worth checking
If it’s high
A result of 50 mg/dL or higher is considered high by several guidelines. Risk rises gradually as the level goes up. The 2026 US guideline links about 125 nmol/L (roughly 50 mg/dL) to about 1.4 times the risk of heart and blood vessel disease, and about 250 nmol/L (roughly 100 mg/dL) to about double. The mg/dL figures are only rough, because the two units can't be converted exactly. A high level raises risk but does not mean a heart attack or stroke will happen. Your overall risk also depends on your age, blood pressure, LDL cholesterol, smoking and family history.
Common causes
- Your genes. Variation in the LPA gene explains more than 90% of the differences between people
- Ancestry. Average levels differ between groups and tend to be higher in people of South Asian and African ancestry
- Kidney disease, especially nephrotic syndrome, which can raise levels 3 to 5 times
- An underactive thyroid (hypothyroidism)
- Pregnancy, when levels can roughly double
- Some inflammatory conditions and some HIV medicines
What can help
- Because Lp(a) is mostly genetic, lifestyle changes move it only a little. They still lower your overall heart risk
- Work on the risk factors you can change: blood pressure, LDL cholesterol, blood sugar, weight, activity and smoking
- Ask your clinician how your Lp(a) fits with your overall heart risk
- Ask whether close relatives should have their Lp(a) checked, since it runs in families
Usual ranges
What labs print as the reference range, by who was tested. Ranges differ a little between labs, so the range on your own report is the one your result is judged against.
For adults: up to 29.9 mg/dL. Source: European Heart Journal.
- Adults (this one applies)up to 29.9 mg/dL
Source: European Heart Journal
EAS 2022 consensus Lp(a) thresholds (50 mg/dL also used by 2018 AHA/ACC and 2026 ACC/AHA)
- Below 30: lower Lp(a)-related riskbelow 30 mg/dL
- Grey zone30 to under 50 mg/dL
- 50 or above: higher Lp(a)-related risk50 and above mg/dL
If this applies to you
Lp(a) mass means a little more for some people. Open the one that fits you.
High cholesterol or heart risk
Some labs report Lp(a) in mg/dL instead of nmol/L. The 2026 U.S. guideline notes that results from different tests and labs are hard to compare, so it helps to compare results in the same unit from the same kind of test.
What can affect your result
- Genes: more than 90% of the differences between people
- Ancestry: average levels are lowest in people of Chinese ancestry and highest in people of African ancestry
- Assay design: antibody-based assays can over- or under-read depending on apo(a) size
- Kidney disease and nephrotic syndrome raise levels; advanced liver disease lowers them
- Thyroid status: an underactive thyroid raises levels and an overactive one lowers them
- Pregnancy can roughly double levels
- Women's levels are on average about 5 to 10% higher than men's
- Fasting and physical activity make little or no difference
- Many antibody-based assays read differently depending on the size of your apo(a) protein, so results from different labs or kits may not match. Use the same lab and assay when comparing over time.
- Labcorp notes that alcohol, aspirin, niacin and estrogen supplements may misrepresent true Lp(a); tell your clinician about them.
- Labs may reject grossly hemolyzed, lipemic or icteric samples (Labcorp).
- Kidney disease, thyroid disease, liver disease and pregnancy can shift levels (see factors affecting).
Mostly fixed by your genes. Lifestyle changes have little effect.
When to talk to a clinician
Talk with a clinician about a result of 50 mg/dL or higher, especially if you or close relatives have had a heart attack, stroke or aortic valve problems at a younger age. A level above about 180 mg/dL is linked to a lifetime heart risk similar to that of untreated inherited high cholesterol, so it is worth raising with your clinician soon.
Questions you could ask
- Which assay and units does my lab use for Lp(a), and can I compare this result with earlier ones?
- Do I need to recheck this, or is one result enough?
- How does my Lp(a) fit with my overall risk of heart disease?
- Should my other risk factors, such as LDL cholesterol or blood pressure, be reviewed more closely?
- Should my close relatives have their Lp(a) checked?
- Does my family history change how we should read this result?
Questions people ask
Why is Lp(a) reported in mg/dL on some reports and nmol/L on others?
mg/dL measures the weight of Lp(a), and nmol/L counts the particles. They are different kinds of measurement, and the two can't be converted exactly because the size of the apo(a) protein varies between people and between assays. Experts say 2 to 2.5 is only a rough guess for turning mg/dL into nmol/L. Compare results only in the same unit, ideally from the same lab.
Can diet or exercise lower my Lp(a)?
Very little. Your genes set most of your level, and lifestyle changes have a small effect at most. Healthy habits still lower your overall heart risk, and your clinician may focus on your LDL cholesterol, blood pressure and other factors.
Do I need to test Lp(a) more than once?
Often one test is enough, because the level is steady over time. Several guidelines suggest measuring it at least once in adulthood. Your clinician may repeat it if the first result was close to a cutoff or if your health changes.
Is Lp(a) already included in my LDL number?
Partly. The cholesterol inside Lp(a) particles is counted within standard LDL cholesterol, so a high Lp(a) can make your LDL look a bit higher than the LDL particles alone. Some labs can report an LDL adjusted for this, and your clinician can tell you whether that matters for you.
What counts as a high Lp(a) in mg/dL?
Several guidelines use 50 mg/dL as the point where risk is considered higher, with a grey zone from 30 to 50 mg/dL. Risk rises gradually as the number goes up, so there is no single line between safe and unsafe. Your lab's own cut-offs may be different, especially if its assay is calibrated in different units.
Show the science and sources
Units
- 1 mg/dL = 1 mg/dL
- 1 mg/dL = 10 mg/L
- 1 mg/dL = 0.01 g/L
Open the Lp(a) mass unit converter
Is a change real?
Lp(a) mass naturally varies about 8.9% from test to test in the same healthy person. Between two results from the same lab, a rise of 30% or more, or a fall of 23% or more, is unlikely to be day-to-day noise or lab variation (95% reference change value). Source: The European Biological Variation Study (EuBIVAS): a summary report.
For clinicians and researchers
Lp(a) is an LDL-like particle whose apoB-100 is linked to apolipoprotein(a), encoded by LPA. Concentration ranges from under 0.1 to over 300 mg/dL, is more than 90% genetically determined, and is inversely related to apo(a) isoform size (the number of kringle IV repeats explains about 30-70% of the variation). Most commercial immunoassays use polyclonal antibodies that recognize repeated epitopes, so mass-based results can read low in small isoforms and high in large ones; isoform-insensitive assays traceable to official reference materials and reported in nmol/L are preferred. The EAS 2022 consensus advises against a fixed mg/dL to nmol/L factor (2 to 2.5 is only a best guess; it uses 2.5 as an interim figure), and the 2026 ACC/AHA guideline treats the units as not directly interchangeable. Thresholds: EAS 2022 suggests a rule-out level below 30 mg/dL (75 nmol/L), a rule-in level of 50 mg/dL (125 nmol/L) or more, and a grey zone between; the 2018 AHA/ACC guideline names 50 mg/dL or 125 nmol/L a risk-enhancing factor; the 2026 ACC/AHA guideline recommends measurement at least once in adulthood and, using nmol/L thresholds, links about 125 nmol/L to about 1.4-fold, about 250 nmol/L to about 2-fold and about 430 nmol/L to about 4-fold relative ASCVD risk (as summarized in Life 2026; mg/dL equivalents are approximate). The EAS/EFLM 2016 statement suggested lab flags at 50 mg/dL or more (about the 80th percentile) and specialist referral above 150 mg/dL (99th percentile). Above 180 mg/dL (430 nmol/L) lifetime ASCVD risk is similar to untreated heterozygous familial hypercholesterolemia. The relation is causal and continuous for ASCVD and aortic valve stenosis, and does not support Lp(a) as a venous thrombosis risk factor. Lp(a) carries cholesterol that is measured inside LDL-C (about 30-45% of Lp(a) mass on average, but 6-60% between people); the EAS does not recommend routine correction of LDL-C except where familial hypercholesterolemia is suspected. Hormone therapy after menopause lowers Lp(a) by about 25%, and PCSK9 inhibitors lower it by 15-30% (EAS).
LOINC 10835-7 (primary). Specimen: serum-or-plasma.
Sources
- Lipoprotein(a) in atherosclerotic cardiovascular disease and aortic stenosis: a European Atherosclerosis Society consensus statement, European Heart Journal (2022)
- 2018 AHA/ACC/AACVPR/AAPA/ABC/ACPM/ADA/AGS/APhA/ASPC/NLA/PCNA Guideline on the Management of Blood Cholesterol, Circulation (2018)
- 2026 ACC/AHA/AACVPR/ABC/ACPM/ADA/AGS/APhA/ASPC/NLA/PCNA Guideline on the Management of Dyslipidemia, American College of Cardiology / American Heart Association (2026)
- The 2026 ACC/AHA Dyslipidemia Guideline: A Critical and Transatlantic Perspective on Personalized Lipid Management, Life (MDPI) (2026)
- Prioritizing Health | Lower Sooner: How the 2026 Dyslipidemia Guideline Changes Practice, American College of Cardiology (2026)
- Fasting is not routinely required for determination of a lipid profile: clinical and laboratory implications including flagging at desirable concentration cut-points (EAS and EFLM joint consensus statement), European Heart Journal (2016)
- Lipoprotein(a) (test 120188), Labcorp
- Lipoprotein (a) and Low-Density Lipoprotein Cholesterol, Serum (test LPALD), Mayo Clinic Laboratories
- Lipoprotein (a) Blood Test, MedlinePlus (National Library of Medicine)
AI-verified against cited sources. Awaiting expert review. Last reviewed 2026-10-03. How we build and check these pages.