The Anti‐platelet Effect of Aspirin in Patients with End Stage Renal Disease

Abstract

Aspirin (ASA) resistance, a biochemical in vitro phenomenon in which ASA ingestion fails to inhibit platelet aggregation, likely explains the recurrence of vascular events in subjects taking ASA. The objective here was to determine the effect of renal failure on the anti-platelet effect of ASA. Renal failure and control subjects taking ASA alone were compared. Using three distinct platelet agonists, soluble collagen (2 microg/ml), ADP (5 microM) and arachidonic acid (AA) (0.164 mM), platelet aggregation was quantified (Ohms) in whole blood (Chrono-log, Havertown, PA). Both renal failure and control patients exhibit variable response to ASA with subjects showing potent agonist-induced platelet aggregation at the extreme, consistent with the existence of ASA resistance. The average extent of aggregation in response to collagen (renal failure: 7.78 ± 0.69, n=13 vs. control 8.9 ± 0.64, n=39, mean ± SEM in Ohms) and ADP (renal: 10.4 ± 1.67, n=13 vs. control: 10.54 ± 0.91, n=39) was similar between the two groups (P>0.1). In response to AA, the natural substrate of cyclooxygenase at which ASA inhibits, renal failure patients showed a significantly greater platelet aggregation than did the control patients (renal failure: 7.84 ± 1,28 n=13 vs. control: 5.04 ± 0.69, n=24, p=0.044, two-sample unpaired t test). The variance of the increase in aggregation by the three agonists between both groups was similar (P>0.1). These data imply an attenuated anti-platelet response to ASA.