title: Outcome and causes of renal deterioration evaluated by serial cystatin C measurements in acute coronary syndrome patients -- results from the PLATelet inhibition and patient Outcomes (PLATO) study.
abstract: BACKGROUND
  To investigate if ticagrelor treatment and other clinical characteristics were associated with increased cystatin C concentrations and if a deterioration in estimated renal function was associated with worse outcome in patients with acute coronary syndromes (ACS).
  
  
  METHODS
  Plasma cystatin C concentrations were determined within 24 hours of admission (baseline), at discharge, 1 month, and 6 months in the PLATO trial. The changes over time in relation to randomized treatment were analyzed by analysis of covariance. C-statistics and the relative Integrated Discrimination Improvement of the cystatin C concentrations regarding the primary outcome (cardiovascular death or myocardial infarction) was evaluated by multivariable analysis including background characteristics and biomarkers: N-terminal-pro-B-type natriuretic peptide and Troponin I.
  
  
  RESULTS
  Mean cystatin C concentrations in 2133 ticagrelor- and 2162 clopidogrel-treated patients were at baseline (0.86 mg/L and 0.86 mg/L), discharge (1.01 mg/L and 0.98 mg/L) (P < .0005), 1 month (1.00 mg/L and 0.98 mg/L) (P = .12), and 6 months (1.00 mg/L and 0.99 mg/L) (P = .17), respectively. Age, heart failure, and type of ACS were major determinants of the cystatin C concentration. c Statistics and the relative Integrated Discrimination Improvement of the primary outcome for the baseline cystatin C concentration were 0.687 and 5.2%, compared to 0.684 and 4.5% at discharge (n = 4034) and 0.693 and 5.1% at one month (n = 3096), respectively.
  
  
  CONCLUSIONS
  Mean cystatin C concentrations increased in ACS patients, most importantly determined by age. The initial greater increase in ticagrelor-treated patients was not sustained over time. Risk prediction did not improve with serial measurements of renal markers.
authors.affiliation: Uppsala Clinical Research Center, Uppsala University, Uppsala, Sweden. axel.akerblom@ucr.uu.se
authors.forename: Axel
authors.initials: A
authors.lastname: Akerblom
authors.forename: Lars
authors.initials: L
authors.lastname: Wallentin
authors.forename: Agneta
authors.initials: A
authors.lastname: Siegbahn
authors.forename: Richard C
authors.initials: RC
authors.lastname: Becker
authors.forename: Andrzej
authors.initials: A
authors.lastname: Budaj
authors.forename: Jay
authors.initials: J
authors.lastname: Horrow
authors.forename: Steen
authors.initials: S
authors.lastname: Husted
authors.forename: Hugo
authors.initials: H
authors.lastname: Katus
authors.forename: Marc J
authors.initials: MJ
authors.lastname: Claeys
authors.forename: Robert F
authors.initials: RF
authors.lastname: Storey
authors.forename: Nils
authors.initials: N
authors.lastname: Asenblad
authors.forename: Stefan K
authors.initials: SK
authors.lastname: James
mesh_terms: D054058:Acute Coronary Syndrome / Q000097:blood* / Q000188:drug therapy* / Q000378:metabolism; D000241:Adenosine / Q000031:analogs & derivatives* / Q000627:therapeutic use; D000368:Aged; D000704:Analysis of Variance; D015415:Biomarkers / Q000097:blood; D000077144:Clopidogrel; D055316:Cystatin C / Q000097:blood* / Q000378:metabolism; D005260:Female; D006801:Humans; D007668:Kidney / Q000187:drug effects / Q000378:metabolism*; D007677:Kidney Function Tests; D008297:Male; D008875:Middle Aged; D010975:Platelet Aggregation Inhibitors / Q000627:therapeutic use*; D058921:Purinergic P2Y Receptor Antagonists / Q000627:therapeutic use; D012307:Risk Factors; D000077486:Ticagrelor; D013988:Ticlopidine / Q000031:analogs & derivatives* / Q000627:therapeutic use; D016896:Treatment Outcome
chemical_list: D015415:Biomarkers; D055316:Cystatin C; D010975:Platelet Aggregation Inhibitors; D058921:Purinergic P2Y Receptor Antagonists; D000077144:Clopidogrel; D000077486:Ticagrelor; D000241:Adenosine; D013988:Ticlopidine