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Am J Cardiol. 2016 Feb 15;117(4):656-663. doi: 10.1016/j.amjcard.2015.11.029. Epub 2015 Dec 7.

Differences in Whole Blood Platelet Aggregation at Baseline and in Response to Aspirin and Aspirin Plus Clopidogrel in Patients With Versus Without Chronic Kidney Disease.

Author information

1
Department of Internal Medicine, Kidney Institute, University of Kansas Medical Center, Kansas City, Kansas.
2
Division of Biostatistics, Department of Clinical Sciences, University of Texas Southwestern Medical Center, Dallas, Texas.
3
Department of Pathology, University of Texas Southwestern Medical Center, Dallas, Texas.
4
Division of Nephrology, Department of Internal Medicine, University of Texas Southwestern Medical Center, Dallas, Texas.
5
Division of Cardiology, Department of Internal Medicine, University of Texas Southwestern Medical Center, Dallas, Texas; Division of Cardiology, Department of Internal Medicine, Veterans Affairs North Texas Health Care System, Dallas, Texas.
6
Division of Nephrology, Department of Internal Medicine, University of Texas Southwestern Medical Center, Dallas, Texas; Division of Nephrology, Department of Internal Medicine, Veterans Affairs North Texas Health Care System, Dallas, Texas. Electronic address: susan.hedayati@utsouthwestern.edu.

Abstract

Thrombotic events while receiving antiplatelet agents (APAs) are more common in subjects with versus without chronic kidney disease (CKD). Data on antiplatelet effects of APA in CKD are scarce and limited by lack of baseline platelet function before APA treatment. We hypothesized subjects with stages 4 to 5 CKD versus no CKD have greater baseline platelet aggregability and respond poorly to aspirin and clopidogrel. In a prospective controlled study, we measured whole blood platelet aggregation (WBPA) in 28 CKD and 16 non-CKD asymptomatic stable outpatients not on APA, frequency-matched for age, gender, obesity, and diabetes mellitus. WBPA was remeasured after 2 weeks of each aspirin and aspirin plus clopidogrel. The primary outcome was percent inhibition of platelet aggregation (IPA) from baseline. The secondary outcome was residual platelet aggregability (RPA; proportion with <50% IPA). Baseline platelet aggregability was similar between groups except adenosine diphosphate-induced WBPA, which was higher in CKD versus non-CKD; median (interquartile range) = 13.5 (9.5 to 16.0) versus 9.0 (6.0 to 12.0) Ω, p = 0.007. CKD versus non-CKD participants had lower clopidogrel-induced IPA, 38% versus 72%, p = 0.04. A greater proportion of CKD versus non-CKD participants had RPA after clopidogrel treatment (56% vs 8.3%, p = 0.01). There were no significant interactions between CKD and the presence of cytochrome P450 2C19 polymorphisms for platelet aggregability in clopidogrel-treated participants. In conclusion, CKD versus non-CKD subjects exhibited similar platelet aggregation at baseline, similar aspirin effects and greater RPA on clopidogrel, which was independent of cytochrome P450 2C19 polymorphisms.

TRIAL REGISTRATION:

ClinicalTrials.gov NCT01768637.

PMID:
26725101
PMCID:
PMC4738090
DOI:
10.1016/j.amjcard.2015.11.029
[Indexed for MEDLINE]
Free PMC Article

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