Key result
Moderate to severe chronic kidney disease was associated with a significantly higher likelihood of high on-treatment platelet reactivity to aspirin compared to normal or mildly diminished kidney function (48% vs. 23%; OR 3.17).
Why the study?
Chronic kidney disease has been hypothesized to influence pharmacological responsiveness to antiplatelet drugs, prompting this evaluation of how aspirin affects blood clotting in CKD sufferers.
Does chronic kidney disease reduce the antiplatelet activity of aspirin in patients taking aspirin regularly?
Cross-Sectional (n=120)
No
Does chronic kidney disease reduce the antiplatelet activity of aspirin in patients taking aspirin regularly?
Chronic kidney disease is associated with a higher likelihood of high on-treatment platelet response to aspirin, suggesting compromised antiplatelet efficacy in this population.
Should not yet change aspirin use in CKD; leaves open whether reactivity predicts ischemic events.
Background and aim: Individual differences in the pharmacological responsiveness to aspirin are considerable. A higher likelihood of ischemic episodes is linked to aspirin's inadequate antiplatelet actions. It has been hypothesized that chronic kidney disease (CKD) influences the pharmacologic reaction to antiplatelet drugs. The elevated chance of fatality and cardiovascular problems in CKD sufferers has already been found to be largely explained by high on-treatment platelets response (HTPR) to clopidogrel. This research aimed to examine at how aspirin affects blood clotting in CKD sufferers. Method: We performed cross-sectional research on 120 people in Medical center of Lahore taking aspirin regularly. The thromboxane production generated by AAI was used to gauge the pharmacologic reaction to aspirin. Result: Individuals with poor kidney functioning were more likely to experience HTPR to aspirin (48% vs. 23%; odds ratio, 3.17; 95% confidence interval [CI], 1.35-7.42; P = 0.007). When compared to individuals with healthy or mildly diminished kidney performance, those with mild or serious CKD had lower pharmacokinetic responsiveness to aspirin (91; interquartile ranged [IQR], 281 ng mL-1; differential in medians, 56; CI, 6-110 ng mL-1; P = 0.012). Remaining thromboxane production and glomerular filtration rate were both associated by bivariate Pearson correlation analysis (R = 0.312; R2 = 0.093; P = 0.001). Individuals with CKD were usually old age and being women. Women and aged were not significant predictors of the connection, according to multivariate linear regression analyses (R = 0.313; R2 = 0.081; P = 0.002 and P = 0.006) respectively. Conclusion: Aspirin pharmacological reaction is associated with kidney function. Individuals who have CKD are more likely to have aspirin's antiplatelet action compromised. To evaluate the therapeutic significance of this data and look into the best antithrombotic strategy for CKD individuals, additional research is required.
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Saqib Ali (2022) conducted a cross-sectional in Chronic Kidney Disease (n=120). Moderate to severe chronic kidney disease vs. Normal or mildly diminished kidney function was evaluated on High on-treatment platelet response (HTPR) to aspirin (OR 3.17, 95% CI 1.35-7.42, p=0.007). Moderate to severe chronic kidney disease was associated with a significantly higher likelihood of high on-treatment platelet reactivity to aspirin compared to normal or mildly diminished kidney function (48% vs. 23%; OR 3.17).
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