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Hemodialysis Blunts the Anti‐platelet Effect of Aspirin and Can Contribute to Aspirin Resistance in Patients with End‐stage renal disease
Author(s) -
Malay Rajya,
Faheem Osman,
Azrin Michael,
Kaplan Andre,
Schumacher Jayne,
Kupiec Jessica,
Liang Bruce
Publication year - 2007
Publication title -
the faseb journal
Language(s) - English
Resource type - Journals
SCImago Journal Rank - 1.709
H-Index - 277
eISSN - 1530-6860
pISSN - 0892-6638
DOI - 10.1096/fasebj.21.5.a439-c
Subject(s) - aspirin , platelet , arachidonic acid , hemodialysis , adenosine diphosphate , cyclooxygenase , medicine , chemistry , end stage renal disease , dialysis , endocrinology , platelet aggregation , pharmacology , biochemistry , enzyme
Aspirin (ASA) resistance, a biochemical in vitro phenomenon in which ASA ingestion fails to prevent platelet aggregation, has been well described. The effects of renal failure and hemo‐dialysis (HD) on the anti‐platelet response to ASA are not known. The objective here was o test the hypothesis that HD alters the anti‐platelet effect of ASA in patients with ESRD. Twenty three consecutive ESRD patients on ASA were enrolled and agonist‐stimulated platelet aggregation determined before and after HD. Whole blood aggregometry (WBA) was performed and platelet aggregation was quantified as an increase in resistance (Ohms) (Chrono‐log, Havertown, PA) in response to three standard agonists: soluble collagen (2 microg/ml), ADP (5 microM) and arachidonic acid (AA) (0.164 mM). In response to AA before HD, the natural substrate of cyclooxygenase that is in turn the target of inhibition by ASA, patients on ASA showed a significantly lower aggregation than patients not taking ASA (6.2 ± 0.46 ohms, SEM, n=23 vs. 8.23 ± 1.04 ohms, n=9, P<0.05), consistent with an ASA‐mediated anti‐platelet effect. After HD, patients on ASA showed a significantly greater AA‐stimulated platelet aggregation (6.2 ± 0.46 ohms vs. 7.98 ± 0.77 ohms, n=23, Wicoxon matched pair test, P=0.022). In contrast, HD had no effect on the AA‐stimulated aggregation in patients not taking ASA (termed no‐ASA group) (P>0.1). The extent of aggregation in response to collagen and adenosine diphosphate (ADP) was similar before and after HD in both ASA and no‐ASA groups (P>0.1). Conclusions: HD enhanced AA‐induced platelet aggregation in patients on ASA but was without effect on ESRD patients not taking ASA. HD blunts the anti‐platelet effect of ASA and can contribute to ASA resistance in this patient group.