Lipoprotein (a) is similar to low-density lipoprotein but is unique in having an additional apolipoprotein called apolipoprotein (a) (apo(a)) covalently linked to it. apo(a), which is a member of the plasminogen gene superfamily, has a protease domain which cannot be activated to cause fibrinolysis. Its sequence of kringles is much longer than that of plasminogen and there is remarkable genetic variation in its length. The consequent inherited differences in apo(a) molecular mass are largely responsible for the wide range of serum Lp(a) concentrations in different individuals with low levels predominating in Europid populations. Physiologically Lp(a) may participate in haemocoagulation or in wound-healing. Epidemiological evidence that it is a risk factor for atherosclerosis, particularly in populations with high serum LDL levels, has led to research to uncover its role in atherogenesis and thrombosis. Diseases such as renal disease, and probably atherogenesis and thrombosis. Diseases such as renal disease, and probably atherosclerosis itself, are associated with an increase in Lp(a) above its genetically determined level and it remains a subject of speculation as to whether such increases are as closely involved in atherothrombosis as are spontaneously high levels resulting from low-molecular-mass apo(a) variants.