title: Renal function assessed using cystatin C and antiplatelet efficacy of clopidogrel assessed using the vasodilator-stimulated phosphoprotein index in patients having percutaneous coronary intervention.
abstract: Renal dysfunction is a strong independent predictor of stent thrombosis. The aim of the present study was to evaluate the strength and direction of the association between kidney function and clopidogrel efficacy. The study group consisted of consecutive patients (n = 275) who underwent stent implantation. Drug efficacy was measured using the vasodilator-stimulated phosphoprotein (VASP) index 20 ± 4 hours after clopidogrel 600 mg. Nonresponse was defined as an VASP index ≥50%. Renal function was determined using serum cystatin C. The upper reference levels are 1.12 mg/L for ≤65 years of age and 1.21 mg/L for >65 years of age. Estimated glomerular filtration was calculated using cystatin C. The median value of cystatin C was 1.16 mg/L (twenty-fifth and seventy-fifth percentiles 0.96 and 1.43); 47.63% of the study population had cystatin C above reference levels and 33.1% of patients were nonresponders to clopidogrel. No correlation was found between clopidogrel efficacy assessed with the VASP index and kidney function assessed with cystatin C (Spearman r = -0.070, p = 0.248). Based on cystatin C the proportion of nonresponders to clopidogrel was 34.4% versus 31.9% (p = 0.702) in patients with impaired renal function compared to normal renal function, respectively. The proportion of clopidogrel nonresponders did not differ (p = 0.902) among groups with normal (28.8%), mildly impaired (34.8%), moderately impaired (32.9%), and severely impaired (34.8%) renal function. In conclusion, renal function assessed by cystatin C does not predict clopidogrel efficacy. Renal dysfunction is a complex entity and its significant relation to stent thrombosis cannot be explained simply by a decrease in clopidogrel efficacy.
authors.affiliation: Third Medical Faculty, Charles University, Prague, Czech Republic. zuzana.motovska@iex.cz
authors.forename: Zuzana
authors.initials: Z
authors.lastname: Motovska
authors.forename: Denisa
authors.initials: D
authors.lastname: Odvodyova
authors.forename: Michaela
authors.initials: M
authors.lastname: Fischerova
authors.forename: Sona
authors.initials: S
authors.lastname: Stepankova
authors.forename: Marek
authors.initials: M
authors.lastname: Maly
authors.forename: Petra
authors.initials: P
authors.lastname: Morawska
authors.forename: Petr
authors.initials: P
authors.lastname: Widimsky
mesh_terms: D000368:Aged; D015906:Angioplasty, Balloon, Coronary / Q000379:methods*; D001798:Blood Proteins; D015815:Cell Adhesion Molecules / Q000097:blood*; D000077144:Clopidogrel; D003324:Coronary Artery Disease / Q000503:physiopathology / Q000628:therapy*; D003328:Coronary Thrombosis / Q000097:blood / Q000503:physiopathology / Q000517:prevention & control*; D055316:Cystatin C / Q000097:blood*; D004305:Dose-Response Relationship, Drug; D005260:Female; D005500:Follow-Up Studies; D005919:Glomerular Filtration Rate / Q000187:drug effects / Q000502:physiology*; D006801:Humans; D007118:Immunoassay; D007677:Kidney Function Tests; D008297:Male; D008840:Microfilament Proteins / Q000097:blood*; D010750:Phosphoproteins / Q000097:blood*; D010975:Platelet Aggregation Inhibitors / Q000008:administration & dosage; D011379:Prognosis; D015607:Stents; D013988:Ticlopidine / Q000008:administration & dosage / Q000031:analogs & derivatives*; D000098662:Vasodilator-Stimulated Phosphoprotein
chemical_list: D001798:Blood Proteins; D015815:Cell Adhesion Molecules; D055316:Cystatin C; D008840:Microfilament Proteins; D010750:Phosphoproteins; D010975:Platelet Aggregation Inhibitors; D000098662:Vasodilator-Stimulated Phosphoprotein; D000077144:Clopidogrel; D013988:Ticlopidine