Thromboxane B2 Blood Levels and Incipient System Clotting in Heparin Free Hemodialysis

The effect of selected pre‐analytical phase variables on plasma thromboxane A2 measurements in humans

“…The advantages In this study, we have selected an EIA-based method for direct TxB 2 (11-dTxB 2 ) measurement, because it is still one of the most accessible and suitable methods for the monitoring of the effect of ASA and aspirin response in ASA-treated patients [16]. It is widely known that in healthy donors, the plasma concentrations of TxB 2 (11-dTxB 2 ) are relatively low (1-2 pg/mL TxB 2 ) [17]. ASA treatment dependently of the used dose (100 mg per day is sufficient in 90% of patients to reach the selective cumulative inhibitory effect in low-dose ASA-treated patientsdata not shown) leads to almost 95% reduction in TxB 2 (11-dTxB 2 ) production [18,19].…”

“…These measurements lead us to an interesting observation that trisodium citrate-treated plasma gives concentrations of TxB 2 (11-dTxB 2 ) comparable to those obtained in serum (Figures 1a,b and 2a,b). It is known that higher serum values of TxB 2 (32-64 pg/mL) are attributed to platelet activation, and thus, the ex vivo determination of TxB 2 reflects a maximal capacity of activated platelets to synthesize Tx via COX-1 pathway and it is a most sensitive measure of aspirin response; [17,21] . It was also shown that Tx production does not necessarily correlate with aggregationthis is multifactorial [22].…”

“…It was also shown that Tx production does not necessarily correlate with aggregationthis is multifactorial [22]. On the other hand, the heparinized platelet-rich plasma simulates in vivo conditions and does not refer anything about platelet function in terms of maximal ability to produce Tx [17]. The possible effect of trisodium citrate on the ex vivo platelet activation could be rather interesting and needs further characterization.…”

Physiologic Inhibitors of Coagulation in Patients on Chronic Hemodialysis

“…(4) With the introduction of more sophisticated modes of dialytic therapy, future research could be directed toward the impact of different dialysis membranes and dialysate solutions on hemostasis in ESRD patients. (5) The predictive role of plasminogen activator inhibitor-1 in cardiovascular stability is another area that requires largescale epidemiology surveys. (6) Finally, future studies designed to more precisely define the underlying pathways that account for increased circulating PAI-1 levels would be of great interest to delineate the pathogenic mechanisms that lead to ischemic cardiovascular disease in this group of patients.…”

“…Besides conventional cardiovascular risk factors including diabetes, hypertension, hyperlipidemia, secondary hyperparathyroidism, hypoalbuminemia, smoking, and sedentary lifestyle, increasing attention has also been paid to the role of hemostatic factors. The regular contact of blood with bioincompatible dialyzer membranes induces platelet activation [5], plasma coagulation [6], and alterations in the physiologic inhibitors of coagulation. Over the past decade, there has been steady, albeit sluggish, progress in the understanding of the impact of chronic hemodialysis on endogenous plasma coagulation inhibitors.…”