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How important coadministration of antiplatelet agents is in the pathogenesis of some of these hemorrhagic events is unclear in the context of uremic platelet dysfunction. Antiplatelet agents were administered to 7 of our 10 patients and 1
of the 5 cases described. However, their use would not explain the prolonged APTT seen in 7 of our 10 cases. Four of our patients were on the maintenance hemodialysis program; although the onset of bleeding was on nondialysis days in all
patients and the quoted APTTs were 48 hours after hemodialysis, the possible contribution of heparin during dialysis treatment remains unclear. Finally, in our case series, 7 of 10 patients had end-stage renal disease (ESRD), but 1 patient
had a CrCl of 30 mL/min (0.50 mL/s) and still experienced a major hemorrhagic event (Fig1). Although there was an overlap with warfarin therapy, he had only been administered 2 doses,and his international normalized ratio was 2.4.
LMWHs are derived from standard UFH through controlled chemical or enzymatic degradation, resulting in heterogeneous molecules with individual pharmacological properties. Each commercial product is considered by theWorld Health Organization as a distinct and noninterchangeable drug. There are important differences between
LMWHs and UFH, but the clinical relevance of their differences in terms of effectiveness or safety remains unclear. Hence, LMWHs have a reduced ability to catalyze the inhibition of thrombin (IIa), whereas they retain the ability to inhibit Xa activity. The reduced binding of LMWH to plasma proteins and cells (including platelets, endothelial cells, and macrophages) contributes to its more predictable dose response and longer plasma half-life. LMWHs are eliminated primarily by the kidney through glomerular filtration in comparison to UFH, in which renal clearance becomes an important route of elimination only at greater concentrations.

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