Lipoprotein(a) — “Lp(a)” — is an inherited, largely fixed cholesterol particle that roughly one in five people carry at a level high enough to raise their cardiovascular risk independently of everything else. As of 2026, both US and European guidelines recommend measuring it at least once in every adult’s life. The catch is that labs report it in two different units — nmol/L and mg/dL — that don’t convert cleanly. This tool gives an approximate conversion and, more usefully, tells you which risk band your result sits in.
Get a result in nmol/L if you can
nmol/L measures the number of Lp(a) particles; mg/dL measures their mass. Because particle size varies from person to person, there is no reliable factor between them — and current guidance (the 2024 National Lipid Association update and the European Atherosclerosis Society) explicitly advises against using a fixed conversion factor for clinical decisions. So: treat any converted value below as a rough ballpark only (this tool uses ~2.15 nmol/L per mg/dL), and where possible ask your lab to report Lp(a) directly in nmol/L, now the preferred unit.
Risk bands, guidance & therapies on the horizon
Bands reflect current guidance (2024 National Lipid Association focused update; 2026 ACC/AHA dyslipidemia guideline; 2022 European Atherosclerosis Society consensus): low <75 nmol/L (<30 mg/dL); grey zone 75–125 nmol/L (30–50 mg/dL) — consider a repeat test; high 125–250 nmol/L (50–100 mg/dL); very high ≥250 nmol/L (≥100 mg/dL). Above about 430 nmol/L (180 mg/dL) the lifetime risk can approach that of inherited high cholesterol (familial hypercholesterolaemia). Risk is continuous — these bands are for communication, not biology — and bodies differ slightly (the EAS frames it as one “high” line at ≥50 mg/dL on a continuous scale; HEART UK uses four bands).
Why measure once: Lp(a) is ~80–90% genetically determined and stable through life, so a single accurate reading usually tells you your lifelong level. If it is high, first-degree relatives have roughly a 40–60% chance of also being high — worth family (cascade) screening.
Therapies on the horizon (last reviewed June 2026): no Lp(a)-specific lowering drug is approved yet, and no trial has yet proven that lowering Lp(a) reduces events. The first cardiovascular-outcomes trial, Lp(a)HORIZON (pelacarsen), is expected to report in 2026, with olpasiran, lepodisiran and the oral agent muvalaplin behind it. This note will be updated when results land.
Conversion uses ~2.15 nmol/L per mg/dL — an average only; the true ratio varies with apo(a) particle size, so a value measured directly in nmol/L is always more reliable than a converted one.
Frequently asked questions
How do you convert Lp(a) from nmol/L to mg/dL?
There is no exact conversion: nmol/L counts particles while mg/dL measures mass, which varies with particle size. A rough average is about 2.15 nmol/L per mg/dL, but guidelines advise getting a direct nmol/L lab result rather than converting.
What Lp(a) level is high?
Broadly, under 75 nmol/L (30 mg/dL) is low, 75–125 nmol/L (30–50 mg/dL) is a grey zone, and 125 nmol/L (50 mg/dL) or above is high. Above about 430 nmol/L (180 mg/dL), lifetime risk approaches inherited high cholesterol.
How often should lipoprotein(a) be measured?
Usually just once in a lifetime — Lp(a) is about 80–90% genetic and stays stable. If it is high, first-degree relatives have a 40–60% chance of also being high, so family (cascade) screening is worthwhile.