title: Apolipoprotein B, fibrinogen, HDL cholesterol, and apolipoprotein(a) phenotypes predict coronary artery disease in hemodialysis patients.
abstract: Patients with end-stage renal disease have a markedly elevated risk for coronary artery disease (CAD). Lipids and most lipoproteins, however, seem to be not predictive for CAD in these patients. Although there is clear evidence that lipoprotein(a) [Lp(a)] is significantly elevated in these patients, no study with a sufficiently large group of hemodialysis patients has investigated the relationship between CAD and Lp(a), as well as the genetically determined apolipoprotein(a) [apo(a)] phenotype. This cross-sectional study determines the prevalence of CAD in relation to the cardiovascular risk profile in an unselected population of 607 hemodialysis patients, of which 33% were diabetic patients. Twenty-six percent (n = 158) of all patients suffered from CAD as diagnosed by a definitive myocardial infarction (n = 102) and/or at least one stenosis >50% of a coronary artery (n = 143). In univariate analysis, several classic risk factors, including the concentration of lipids, lipoproteins, apolipoproteins, and fibrinogen, correlated with CAD. Lp(a) in patients with CAD showed only a tendency to higher levels, without reaching significance, compared with patients without CAD (26.6 +/- 30.8 mg/dl versus 22.1 +/- 30.4 mg/dl, P = 0.10). The frequency of low molecular weight apo(a) isoforms, however, was significantly greater in the group with CAD (34.8% versus 23.6%, P < 0.01). Stepwise logistic regression analysis found seven variables associated with CAD: apolipoprotein B, the low molecular weight apo(a) phenotype, male sex, age, fibrinogen, diabetes mellitus, and HDL cholesterol. The association of these variables with CAD differed depending on age. These results indicate that, besides classic risk factors such as age, sex, and diabetes mellitus, additional factors of the lipoprotein and fibrinolytic system contribute to the high prevalence of CAD in hemodialysis patients.
authors.affiliation: Department of Internal Medicine, Heinrich Heine University, Düsseldorf, Germany.
authors.forename: M
authors.initials: M
authors.lastname: Koch
authors.forename: B
authors.initials: B
authors.lastname: Kutkuhn
authors.forename: E
authors.initials: E
authors.lastname: Trenkwalder
authors.forename: D
authors.initials: D
authors.lastname: Bach
authors.forename: B
authors.initials: B
authors.lastname: Grabensee
authors.forename: H
authors.initials: H
authors.lastname: Dieplinger
authors.forename: F
authors.initials: F
authors.lastname: Kronenberg
mesh_terms: D000328:Adult; D000368:Aged; D001055:Apolipoproteins B / Q000097:blood*; D001317:Austria / Q000453:epidemiology; D008076:Cholesterol, HDL / Q000097:blood*; D015897:Comorbidity; D003327:Coronary Disease / Q000453:epidemiology* / Q000209:etiology; D003430:Cross-Sectional Studies; D003920:Diabetes Mellitus / Q000453:epidemiology; D005260:Female; D005340:Fibrinogen / Q000032:analysis*; D006801:Humans; D006973:Hypertension / Q000453:epidemiology; D007676:Kidney Failure, Chronic / Q000097:blood* / Q000150:complications; D017270:Lipoprotein(a) / Q000032:analysis* / Q000235:genetics; D008297:Male; D008875:Middle Aged; D009203:Myocardial Infarction / Q000453:epidemiology / Q000209:etiology; D010641:Phenotype; D015995:Prevalence; D006435:Renal Dialysis; D012307:Risk Factors; D012907:Smoking / Q000453:epidemiology
chemical_list: D001055:Apolipoproteins B; D008076:Cholesterol, HDL; D017270:Lipoprotein(a); D005340:Fibrinogen