Lp(a) was measured in 64 normoalbuminuric, 52 microalbuminuric, and 37
proteinuric Type 1 diabetic patients and 54 healthy subjects. Microal
buminuric and proteinuric Type 1 diabetic patients had higher median L
p(a) values (133 (16-1932) and 169 (17-1149) mg l(-1)) than patients w
ith normal AER (73 (15-1078) mg l(-1); p=0.048 and p=0.027). Lp(a) in
healthy subjects (110 (15-1630)mg l(-1)) did not differ from the diabe
tic subgroups. The frequency of Lp(a) values in the upper quarter of t
he normal distribution was similar in the diabetic groups and did not
differ between diabetic and control subjects. The cumulative distribut
ion of Lp(a) was similar in all groups. Lp(a) concentrations were not
related to AER, age, gender, duration of diabetes, body mass index, gl
ycaemic control, serum creatinine, free insulin or systolic blood pres
sure. Cholesterol, LDL-cholesterol, triglycerides, and apo B were high
er in microalbuminuric and proteinuric than in normoalbuminuric Type 1
diabetic patients. Lp(a) was independently related to diastolic blood
pressure, fibrinogen, and macroangiopathy. In conclusion, median Lp(a
) concentrations tend to be higher in Type 1 diabetic patients with ea
rly and established renal disease, although the differences are small
and the overlap between groups large. Lp(a) is related to diastolic bl
ood pressure and fibrinogen, and this association of powerful risk fac
tors suggests that Lp(a) may play a role in the pathogenesis of cardio
vascular disease in Type 1 diabetic patients with proteinuria. Whether
Lp(a) is an independent determinant of increased cardiovascular risk
in these patients needs to be elucidated by prospective studies.