Chronic kidney disease (CKD) often coexists with coronary artery disease (CAD), resulting in treatment complications because of altered drug metabolism and efficacy. This study, published in Heart, analyzed the effect of kidney function on the efficacy of two commonly used antiplatelet drugs, clopidogrel and prasugrel, by examining their impact on platelet aggregation in patients with stable CAD.

A total of 164 patients undergoing dual antiplatelet therapy were enrolled and randomly assigned to receive either 75 mg of clopidogrel or 3.75 mg of prasugrel daily. Patients were divided into two groups based on their estimated glomerular filtration rate (eGFR), i.e., those with eGFR below 45 mL/min/1.73 m² and those with eGFR equal to or above this threshold. The primary aim was to assess the level of platelet aggregation inhibition at days 5 and 30 after starting therapy.

Among patients with reduced kidney function (eGFR <45), prasugrel produced a faster decline in platelet aggregation than clopidogrel. At baseline, the mean P2Y12 reaction unit (PRU) values were 198.2 for clopidogrel and 177.2 for prasugrel. By day 5, PRU values were 214.2 for clopidogrel and 157.9 for prasugrel, and on day 30, they were 200.0 and 141.7, respectively.

The difference in PRU on day 5 was statistically significant (p=0.036), but not on day 30 (p=0.105). The interaction between drug effect and eGFR was significant only on day 5 (p=0.028), indicating that kidney function influenced drug efficacy mainly in the early treatment phase.