# Influence of Chronic Kidney Disease on Platelet Reactivity Response to Clopidogrel and Ticagrelor

**Authors:** André Franci, Roberto Giraldez, Carlos Barbosa, Talia Dalçóquio, Paulo Genestreti, Aline Ferrari, Fernando Menezes, Remo Furtado, Danilo Sarti, Luciano Baracioli, José Nicolau

PMC · DOI: 10.3390/ijms27031359 · International Journal of Molecular Sciences · 2026-01-29

## TL;DR

Chronic kidney disease reduces the effectiveness of clopidogrel in preventing blood clots, but not ticagrelor, making ticagrelor a better option for patients with kidney disease.

## Contribution

This study shows that CKD impairs clopidogrel's antiplatelet effect but not ticagrelor's, highlighting ticagrelor's potential advantage in CKD patients.

## Key findings

- CKD patients on clopidogrel had higher platelet reactivity compared to those without CKD.
- Ticagrelor showed similar platelet reactivity in both CKD and non-CKD patients.
- HPR was significantly more common with clopidogrel, especially in CKD patients.

## Abstract

High platelet reactivity (HPR) in patients with coronary artery disease receiving P2Y12 inhibitors increases ischemic risk. Chronic kidney disease (CKD) is an established contributor to HPR during clopidogrel therapy. The objective of the study was to assess whether CKD influences platelet reactivity (PR) in patients treated with clopidogrel or ticagrelor. This double-blind, double-dummy study enrolled 106 stable patients more than one year after an acute coronary syndrome, with or without CKD. Participants were matched by age and sex and randomized to clopidogrel or ticagrelor. PR was measured using the VerifyNow™ P2Y12 assay, and HPR was defined as P2Y12 reaction units (PRU) ≥ 208. Median glomerular filtration rates were 80 mL/min/1.73 m2 in non-CKD patients and 41 mL/min/1.73 m2 in CKD patients (p < 0.01). Ticagrelor produced similarly low PR in both groups (36 vs. 35 PRU; p = 0.61). Clopidogrel resulted in a numerically higher PR in CKD patients (209 vs. 180 PRU; p = 0.07). The magnitude of PR reduction with ticagrelor relative to clopidogrel was greater in CKD patients (p-interaction = 0.09). HPR was markedly more common with clopidogrel, particularly in CKD (difference 37%; adjusted OR 4.42; p = 0.01). In conclusion, CKD significantly impairs clopidogrel responsiveness but does not affect ticagrelor, resulting in a greater relative advantage of ticagrelor in patients with CKD.

## Linked entities

- **Chemicals:** clopidogrel (PubChem CID 2806), ticagrelor (PubChem CID 9871419)
- **Diseases:** chronic kidney disease (MONDO:0005300), coronary artery disease (MONDO:0005010), acute coronary syndrome (MONDO:0005542)

## Full-text entities

- **Genes:** P2RY12 (purinergic receptor P2Y12) [NCBI Gene 64805] {aka ADPG-R, BDPLT8, HORK3, P2T(AC), P2Y(12)R, P2Y(AC)}
- **Diseases:** CKD (MESH:D051436), coronary artery disease (MESH:D003324), ischemic (MESH:D002545), acute coronary syndrome (MESH:D054058)
- **Chemicals:** Clopidogrel (MESH:D000077144), Ticagrelor (MESH:D000077486)
- **Species:** Homo sapiens (human, species) [taxon 9606]

## Full text

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## Figures

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## References

39 references — full list in the complete paper: https://tomesphere.com/paper/PMC12897854/full.md

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Source: https://tomesphere.com/paper/PMC12897854