The nephrotic syndrome is frequently associated with hyperlipidaemia a
nd hyperfibrinogenaemia, leading to an increased coronary and thrombot
ic risk, which may be enhanced by high lipoprotein (a) [Lp(a)] concent
rations. We followed the quantitative and qualitative pattern of plasm
a lipoproteins over 18 months in a patient with nephrotic syndrome suf
fering from premature coronary artery disease and with elevated level
of Lp(a) (470 mg dL(-1)). Analysis of kinetic parameters after heparin
-induced extracorporeal plasma apheresis revealed a reduced fractional
catabolic rate for both low-density lipoprotein (LDL and Lp(a). After
improvement of the nephrotic syndrome, Lp(a) decreased to 169 mg dL(-
1) and LDL concentrations were normalized. The decrease of Lp(a) was a
ssociated with an increase in plasma albumin concentrations. Analysis
of apo(a) isoforms in the patient showed the presence of isoform S2 (a
lleles 10 and 19), Consequently, the authors' present strategy is to n
ormalize the elevated Lp(a) and fibrinogen levels. For this purpose he
parin-mediated extracorporeal LDL precipitation (HELP) apheresis is a
promising regimen, helping to reduce the thrombotic risk and prevent c
oronary and graft atherosclerosis as well as the progression of glomer
ulosclerosis in our patient.