What is lp(a)?
Lipoprotein(a), Lp(a) for short, is an LDL particle with an extra protein attached to it, apolipoprotein(a). That protein closely resembles plasminogen, a protein that dissolves blood clots, and it gets in the way of that dissolving. As a result an Lp(a) particle does two things at once: it carries cholesterol into the artery wall, like any LDL particle, and it promotes inflammation and clotting at the spot where it lodges. How much Lp(a) you produce is set for more than 90 percent by a single gene. The value is largely fixed in early childhood and barely changes afterwards, not with diet, weight or exercise either. Because Lp(a) is an LDL particle, the cholesterol it carries counts in your total cholesterol and in your non-HDL, without appearing separately. A raised Lp(a) therefore stays invisible in an ordinary fat profile: it sometimes explains why someone with a tidy LDL still develops cardiovascular disease young, or why it runs strikingly often in a family. Your report shows Lp(a) as one number, in nmol/L or in g/L depending on your lab, and those units cannot be converted exactly; so read your result beside your own lab's threshold. The table further down sets those thresholds side by side.
Why is lp(a) relevant?
A high Lp(a) raises the risk of a heart attack, a stroke and of narrowing of the aortic valve, and that link is causal: people with an inherited high Lp(a) get those diseases more often, independently of all their other risk factors. It is one of the few inherited risk factors you can see with a single blood test, and because the value is stable for life, that in principle needs doing only once. For anyone who wants to stay healthy that is the value of this test: knowing once whether you carry this trait, so that for the rest of your life you know how strict to be with the other risk factors. What you can do about the number itself is limited, and that is the honest side of this story. Lifestyle barely moves Lp(a), and there is no approved drug yet that lowers it specifically; drugs for that are being studied. What you can do, and what demonstrably reduces the risk, is tackle the rest of your risk more strictly: keep LDL low with food and exercise, a healthy blood pressure, no smoking, a healthy weight. That is why the European expert panel advises measuring Lp(a) once in every adult, while the Dutch guideline for now considers it only at moderately increased risk, in unexplained early vascular disease and with early cardiovascular disease in the family.
Lp(a) decision limits
What counts alongside the number:
- The unit on your report and your own lab's threshold, because they differ
- LDL, blood pressure, weight and smoking: with a high Lp(a) those are the levers that do exist
- Cardiovascular disease at a young age in the family, the classic reason to measure Lp(a)
- A temporary cause such as pregnancy, a slow thyroid or kidney disease
Every row is a threshold, not a range a healthy person is supposed to fall inside: no lab publishes a measured distribution for Lp(a). Unilabs and Star-shl report in nmol/L, Clinical Diagnostics and Certe in a mass unit, and between those two there is no fixed conversion factor because the tests differ. So read your result beside the threshold in the same unit; the European panel writes its thresholds in both units, and there 75 nmol/L goes with 0.30 g/L.
What Dutch labs actually use
Two labs work in nmol/L and two in a mass unit, and within neither pair do they agree. Star-shl sets the threshold at 75 nmol/L, the value the European panel pairs with 0.30 g/L; Unilabs at 60. In grams per litre, Clinical Diagnostics sits at 0.30 and Certe, with 500 mg/L or 0.50 g/L, higher.
The labs report this value in units that do not convert one to one, so each unit gets its own scale.
In nmol/L
0 – 60nmol/L
Between 60 and 75 it depends on the lab, because each sets its limit on its own method. Above 75 every lab calls it raised.
From 0 – 60 nmol/L no lab calls it raised. Between 60 and 75 it depends on the lab.
In g/L
0.00 – 0.30g/L
Between 0.30 and 0.50 it depends on the lab, because each sets its limit on its own method. Above 0.50 every lab calls it raised.
From 0.00 – 0.30 g/L no lab calls it raised. Between 0.30 and 0.50 it depends on the lab.
Every age, per lab
| Laboratory | Group | Reference range |
|---|---|---|
| Unilabs(Saltro, Medlon, SHO, Atalmedial)2026 | All adults | < 60 nmol/LDecision limit |
| Star-shl2026 | All adults | < 75 nmol/LDecision limit |
| Certe2026 | From 18 yrs | < 0.50 g/LDecision limitconverted |
| Clinical Diagnostics2026 | All adults | <0.30 g/LDecision limit |
Each band as the lab publishes it, retrieved in 2026, unless marked otherwise.
Lp(a) high or low: what it means
A high Lp(a) is almost always inheritance. Anyone who inherits a small variant of the apo(a) protein makes a lot of it; a large variant gives a low value. On top of that, an underactive thyroid, a pregnancy and kidney disease can raise the value temporarily or lastingly, and hormone therapy after the menopause or a liver disease can lower it. A low Lp(a) is not a problem and asks nothing of you. The European panel works with three bands: below 75 nmol/L (0.30 g/L) a raised Lp(a) is ruled out, above 125 nmol/L (0.50 g/L) it is established, and in between it counts alongside your other risk factors. Do not convert between nmol/L and g/L yourself; the factor differs from test to test. If your Lp(a) is high, the question shifts from this one number to the rest. Every bit of LDL you remove with food and exercise counts for more with a high Lp(a), because your artery wall already has more to bear; the same goes for blood pressure, smoking and weight. Statins do not lower Lp(a) and can even raise it slightly; that is no reason to stop them, because the benefit for your arteries far outweighs that. With a high Lp(a) the useful question is therefore not how to bring this one number down, but how low you keep the rest. And tell your family: the trait is inherited, and one test in a parent, brother or sister says a lot.
What lowers it
Mostly inheritance, and a handful of outside influences.
| Cause | How often |
|---|---|
| InheritanceLarge apo(a) variants go with a lower value | Often |
| Hormone therapy after the menopauseLowers Lp(a) by about a quarter | Sometimes |
| Liver diseaseApolipoprotein(a) is made in the liver | Rare |
What raises it
Here too, mostly inheritance.
| Cause | How often |
|---|---|
| InheritanceSmall apo(a) variants give a markedly higher value; this accounts for by far the largest part | Often |
| Underactive thyroidUnder treatment with thyroid hormone the value falls again | Sometimes |
| PregnancyRoughly a doubling compared with the starting value | Sometimes |
| Kidney diseaseIn nephrotic syndrome a three- to fivefold rise, and the value climbs on dialysis too | Rare |
How does a lp(a) blood test work?
- Referral
- Not needed. You can have Lp(a) measured without going through a doctor first.
- Fasting
- Not needed. Lp(a) does not change with food.
- The draw
- One tube of blood from a vein in your arm, usually at the inner elbow. We measure Lp(a) from a vein; we do not use a finger prick.
- The result
- A single number, at some labs in a mass unit such as grams per litre and at others in nmol/L, next to the threshold that lab uses. The stated turnaround runs from three to fifteen working days.
- Repeating
- Usually not needed: the value is stable for life and repeating does not improve the risk estimate, except with kidney or liver disease or an acute infection. Unilabs reports that Atalmedial applies a five-year lock-out: a new analysis within that term is not run.
- Which test
- Lp(a) is in the Heart health test (€69).
- Where to draw
- You can draw at 350+ locations near you, no referral needed. See the locations
Frequently asked questions
Lp(a) is an LDL particle with an extra protein attached, one that promotes clotting and inflammation in the artery wall. How much of it you have is set almost entirely by your genes and barely changes with lifestyle or diet. That is why the test in principle needs doing only once in your life. That makes Lp(a) different from every other value on these pages.
Related biomarkers
Read on
Sources
- 1.CVRM, Dutch multidisciplinary guideline on cardiovascular risk management, module on estimating cardiovascular risk. 2024. richtlijnendatabase.nl
- 2.CVRM, module on fasting versus non-fasting sampling. 2018. richtlijnendatabase.nl
- 3.EAS, European Atherosclerosis Society consensus statement on lipoprotein(a) in atherosclerotic cardiovascular disease and aortic stenosis. 2022. pmc.ncbi.nlm.nih.gov
- 4.Unilabs, test catalogue (Dutch): lipoprotein(a). 2026. bepalingenklapper.nl
- 5.Star-shl, test catalogue (Dutch): lipoprotein(a). 2026. star-shl.nl
- 6.Certe, test catalogue (Dutch): lipoprotein(a). 2026. bepalingenwijzer.certe.nl
- 7.Clinical Diagnostics, lab guide (Dutch): Lp(a), lipoprotein(a). 2026. clinicaldiagnostics.nl
Educational information only, not medical advice. Consult a healthcare professional for clinical decisions.
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