title: An increased serum level of free Apo(a) in renal patients is more striking than that of Lp(a) and is influenced by homocysteine.
abstract: Lipoprotein(a) [Lp(a)] excess combined with hyperhomocysteinaemia and hyperfibrinogenaemia may contribute to the high incidence of vascular diseases in dialysis patients. This study is aimed at investigating the role of free apolipoprotein(a) [fapo(a)] in renal patients. We have been able to show that, as compared with controls (0.53 mg/l), the median serum concentrations of fapo(a) in patients with nephrotic syndrome (2.58 mg/l) and with peritoneal dialysis (3. 40 mg/l) were strongly elevated (5- to 7-fold), while the fapo(a) levels in patients undergoing haemodialyis (1.02 mg/l) and after renal transplantation (0.90 mg/l) were about doubled. The observed differences in fapo(a) levels indicate that several mechanisms may increase the level of fapo(a), i.e., reduced renal clearance, enhanced hepatic synthesis, or homocysteine releasing apolipoprotein(a) from Lp(a). In the study collective, the median total homocysteine levels were significantly elevated in all patient groups, stronger in patients on haemodialysis (31.4 micromol/l) and peritoneal dialysis (31.2 micromol/l) than in patients with nephrotic syndrome (19.7 micromol/l) and after renal transplantation (19.5 micromol/l). In transplant patients with adequate renal function and without other apolipoprotein(a)-increasing factors, fapo(a) was significantly increased when total homocysteine exceeded 22 micromol/l. In conclusion, our findings let us presume that an increased fapo(a) level in renal patients possibly could be one of the reasons contributing to the high incidence of vascular diseases in these patients, because fapo(a) not covalently linked with Lp(a) is even more easily able to inhibit the fibrinolytic system than the complete Lp(a). These preliminary results have to be confirmed by further investigations.
authors.affiliation: Zentrallabor der Universitätskliniken des Saarlandes, Homburg, Deutschland. kchwher@med-rz.uni-sb.de
authors.forename: W
authors.initials: W
authors.lastname: Herrmann
authors.forename: S
authors.initials: S
authors.lastname: Quast
authors.forename: A
authors.initials: A
authors.lastname: Ellgass
authors.forename: K
authors.initials: K
authors.lastname: Wolter
authors.forename: S T
authors.initials: ST
authors.lastname: Kiessig
authors.forename: E
authors.initials: E
authors.lastname: Molinari
authors.forename: W
authors.initials: W
authors.lastname: Riegel
mesh_terms: D000293:Adolescent; D000328:Adult; D000368:Aged; D000369:Aged, 80 and over; D001054:Apolipoproteins A / Q000097:blood*; D005260:Female; D006710:Homocysteine / Q000097:blood*; D006801:Humans; D020138:Hyperhomocysteinemia / Q000097:blood; D007676:Kidney Failure, Chronic / Q000097:blood* / Q000601:surgery / Q000628:therapy; D016030:Kidney Transplantation; D016014:Linear Models; D017270:Lipoprotein(a) / Q000097:blood*; D008297:Male; D008875:Middle Aged; D009404:Nephrotic Syndrome / Q000097:blood* / Q000601:surgery / Q000628:therapy; D010530:Peritoneal Dialysis; D006435:Renal Dialysis
chemical_list: D001054:Apolipoproteins A; D017270:Lipoprotein(a); D006710:Homocysteine