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RESEARCH PRODUCT

Cholesteryl ester transfer protein activity and cardiovascular events in patients with chronic kidney disease stage V.

Gunnar H. HeineMatthias GirndtXian-cheng JiangKarl WerdanSarah SeilerMichael BuerkeDanilo FliserAxel SchlittC. UlrichKarl J. LacknerStefan Blankenberg

subject

MaleVery low-density lipoproteinmedicine.medical_specialtymedicine.medical_treatmentMyocardial InfarctionKaplan-Meier EstimateSeverity of Illness IndexCohort Studieschemistry.chemical_compoundPredictive Value of TestsRisk FactorsInternal medicineCholesterylester transfer proteinmedicineHumansMyocardial infarctionProspective StudiesAngioplasty Balloon CoronaryCoronary Artery BypassProspective cohort studyStrokeAgedAged 80 and overTransplantationbiologybusiness.industryCholesterolCholesterol HDLMiddle Agedmedicine.diseaseCholesterol Ester Transfer Proteinscarbohydrates (lipids)StrokeEndocrinologychemistryNephrologyChronic Diseasebiology.proteinlipids (amino acids peptides and proteins)FemaleKidney DiseasesStentsHemodialysisbusinessBiomarkersKidney diseaseFollow-Up Studies

description

Background Patients with chronic kidney disease (CKD) have an increased risk for cardiovascular events (CVE). Uraemic dyslipidaemia, which is characterized by low HDL-cholesterol (HDL-C) and elevated triglycerides' levels, may contribute to this elevated cardiovascular risk. Cholesteryl ester transfer protein (CETP) lowers HDL-C by transferring cholesterol esters to LDL and VLDL particles. We tested the hypothesis that CETP activity is associated with CVE in patients with CKD stage V. Methods We measured CETP activity and cholesterol levels in 69 haemodialysis patients. CVE and death were prospectively assessed over a follow-up period of 48 months. Results CETP activity was negatively correlated with HDL-C levels in patients without lipid-lowering medication (r = -0.379, P = 0.005). We found no difference in CETP activity in patients with cardiovascular disease at baseline compared to patients without cardiovascular disease. The same was true for incident CVE during the follow-up. When stratifying patients by median CETP activity, patients with high CETP activity did not have an increased risk for CVE (P = 0.901 by the log-rank test) or death (P = 0.615). Similarly, after stratifying patients by median HDL-C no increased risk for CVE (P = 0.780) or death (P = 0.838) was found in patients with low HDL-C. Conclusions In summary, although CETP activity correlated with HDL-C levels, neither high CETP activity nor low HDL-C was associated with CVE in CKD stage V patients. Thus, pharmacological modification of HDL-C by CETP inhibitors seems to be of questionable value in these patients.

10.1093/ndt/gfn296https://pubmed.ncbi.nlm.nih.gov/18503096