Key result
Kidney transplantation in chronic kidney disease patients on clopidogrel maintenance therapy was associated with a increased risk of high on-treatment platelet reactivity.
Why the study?
Does kidney transplantation and associated immunosuppression increase the prevalence of high on-treatment platelet reactivity in CKD patients receiving maintenance clopidogrel?
Cohort (n=162)
No
Does kidney transplantation and associated immunosuppression increase the prevalence of high on-treatment platelet reactivity in CKD patients receiving maintenance clopidogrel?
Kidney transplantation is independently associated with an increased prevalence of high on-treatment platelet reactivity to clopidogrel, suggesting that platelet function testing may be useful to guide antiplatelet therapy in this high-risk population.
Answers are grounded in this paper and cite their sources.
May warrant platelet testing caution post-transplant in CKD on clopidogrel; leaves open whether testing improves outcomes.
BACKGROUND: Cardiovascular complications represent a major cause of morbidity and mortality for patients who received kidney transplantation (KT). However, the impact of KT and chronic immunosuppression on platelet response to clopidogrel in patients undergoing coronary or peripheral revascularization procedures remains unclear. This cohort study compares platelet responsiveness to clopidogrel as assessed byvasodilator-stimulated phosphoprotein (VASP) phosphorylation. METHODS: The study population was divided between chronic kidney disease (CKD) patients who underwent KT (n = 36) and non-transplanted CKD patients (control group, n = 126). Patients were on maintenance antiplatelet therapy with clopidogrel 75 mg daily for at least 8 days. The mean platelet reactivity index (PRI) VASP values and the prevalence of high on-treatment platelet reactivity (HPR, defined as PRI VASP ≥61 %) were compared. RESULTS: The mean PRI VASP value was significantly higher in the transplant group (60.1 ± 3 vs 51.2 ± 1.6 %; p=0.014). HPR was significantly more common in the transplant group on clopidogrel maintenance therapy (58 vs. 31 %; p = 0.011). KT was the only independent predictor of HPR (odds ratio: 2.6; 95 % confidence interval: 1.03-6.27, p = 0.03). The effect of treatment with calcineurin inhibitors on clopidogrel response could not be analyzed separately from the kidney transplant status. CONCLUSIONS: KT is associated with an increased prevalence of HPR. Our results suggest that plateletfunction tests may be clinically useful for the management of this specific population.
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Müller et al. (2016) conducted a cohort in Chronic kidney disease (n=162). Kidney transplantation vs. Non-transplanted chronic kidney disease patients was evaluated on High on-treatment platelet reactivity (PRI VASP ≥61%) (OR 2.6, 95% CI 1.03-6.27, p=0.03). Kidney transplantation in chronic kidney disease patients on clopidogrel maintenance therapy was associated with a increased risk of high on-treatment platelet reactivity.
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