Extract

Sir,

We read the recently published study by Gritters et al . that evaluated the role of the extracorporeal circuit (ECC) and of the low-molecular-weight heparin (LMWH) in platelet (PLT) activation. Using the PLT surface marker CD62p, they concluded that various parts of ECC are responsible for PLT activation during the haemodialysis (HD) procedure. However, LMWH had no effect on PLT activation, but it contributes to the HD-induced bioincompatibility by releasing platelet factor 4 by the endothelium [ 1 ].

Our team has also evaluated the effect of the HD procedure on PLT function [ 2 ]. We used propyl gallate (PG) slide aggregometry. PG-induced platelet aggregation and tyrosine phosphorylation of multiple proteins are substantially abolished by aspirin, apyrase and abciximab, suggesting that PG is associated with activation of platelet cyclooxygenase 1, adenosine phosphate receptors and GpIIb/IIIa, respectively [ 3 ]. It thus seems that PG is a suitable reagent for a global evaluation of platelet aggregation. We found an effect of the type of dialysis membrane on PLT function and that in HD patients PLT aggregation is impaired. The last is in accordance with the study by Gritters et al . that, considering the lower levels of serotonin in PLTs of HD patients, suggests that repetitive stimulation by HD results in a state of PLT depletion and exhaustion [ 1 ]. However, we found that LMWH affects PLT function in HD patients. A statistically significant negative correlation was almost reached between the dose of tinzaparin sodium, calculated as units/kg of dry body weight and the time needed for platelet aggregation as measured before the start of the HD session ( r = −0.332, P = 0.056). This negative correlation became much stronger and statistically significant after the HD procedure ( r = −0.428, P = 0.009), i.e. near tinzaparin administration indicating a short-term effect of this LMWH on platelet aggregation.

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