title: Apolipoprotein(a) phenotypes predict the risk for carotid atherosclerosis in patients with end-stage renal disease.
abstract: Several studies have demonstrated that atherosclerotic complications are the major cause of morbidity and mortality in hemodialysis patients. High lipoprotein(a) [Lp(a)] plasma concentrations are an independent risk factor for atherosclerosis. Patients with end-stage renal disease (ESRD) have elevated plasma concentrations of Lp(a), which are not explained by size variation at the apolipoprotein(a) [apo(a)] gene locus. The aim of our study was to investigate whether Lp(a) concentrations and/or apo(a) phenotypes are predictive of the degree of atherosclerosis in the extracranial carotid arteries in ESRD patients. Of 167 patients, 108 showed atherosclerotic plaques (65%). Univariate analysis showed that the plaque-affected group was significantly older and had a higher frequency of angina pectoris, previous myocardial infarction, or cerebrovascular accident. Furthermore, this group included significantly more patients with low-molecular-weight apo(a) isoforms (26.9% versus 8.5%, P < .005) and had significantly higher mean Lp(a) plasma concentrations (29.3 +/- 31.0 versus 19.7 +/- 25.7 mg/dL, P < .05). Lp(a) plasma concentration increased significantly with the number of affected arterial sites, from 19.7 mg/dL in patients without plaques to 40.1 mg/dL in patients with seven or eight affected sites. In patients with low-molecular-weight phenotypes, significantly more arterial sites were affected (3.62 versus 2.08, P < .001). Multivariate regression analysis showed that age, angina pectoris, and the apo(a) phenotype were the only significant predictors of the degree of atherosclerosis. We conclude that, besides age, the apo(a) phenotype is the best predictor of carotid atherosclerosis in ESRD patients and may be used for assessment of general atherosclerosis risk in this patient group.
authors.affiliation: Institute of Medical Biology and Human Genetics, Innsbruck, Austria.
authors.forename: F
authors.initials: F
authors.lastname: Kronenberg
authors.forename: H
authors.initials: H
authors.lastname: Kathrein
authors.forename: P
authors.initials: P
authors.lastname: König
authors.forename: U
authors.initials: U
authors.lastname: Neyer
authors.forename: W
authors.initials: W
authors.lastname: Sturm
authors.forename: K
authors.initials: K
authors.lastname: Lhotta
authors.forename: E
authors.initials: E
authors.lastname: Gröchenig
authors.forename: G
authors.initials: G
authors.lastname: Utermann
authors.forename: H
authors.initials: H
authors.lastname: Dieplinger
mesh_terms: D000328:Adult; D000368:Aged; D000369:Aged, 80 and over; D000375:Aging; D000787:Angina Pectoris / Q000150:complications; D001054:Apolipoproteins A / Q000737:chemistry*; D001161:Arteriosclerosis / Q000097:blood*; D002340:Carotid Artery Diseases / Q000097:blood*; D002561:Cerebrovascular Disorders / Q000150:complications; D005260:Female; D006801:Humans; D007676:Kidney Failure, Chronic / Q000097:blood* / Q000150:complications; D008297:Male; D008875:Middle Aged; D008970:Molecular Weight; D015999:Multivariate Analysis; D009203:Myocardial Infarction / Q000150:complications; D010641:Phenotype; D012307:Risk Factors
chemical_list: D001054:Apolipoproteins A