Abstract:
:It is known that thrombosis is a leading cause of vascular access failure and that the formation of thrombus requires platelets. The activation of platelets induces the increase in intracellular Ca 2(+) levels ([Ca(2+)](i)) leading to aggregation and thrombosis. We compared the platelet [Ca(2+)](i) before and after stimulation between the patients with and without easily occluded vascular access. Our study included two groups of hemodialysis patients. Group 1 consisted of 21 patients who had received chronic hemodialysis therapy for more than 6 months. They had had more than three events (including three) of vascular access failures during the past year. Group 2 consisted of 21 hemodialysis patients with age, sex, and diabetes mellitus matched who had never suffered from any event of vascular access failure. We measured the basal and stimulated platelet [Ca(2+)](i) after stimulation with 1 U/ml thrombin, 1 micro M arachidonic acid, 1 micro M platelet activation factor (PAF), and 10 micro M adenosine diphosphate (ADP), respectively. Our results showed that in Ca 2(+)-containing media, there was no significant differences in the basal [Ca(2+)](i), but the maximal increases of [Ca(2+)](i) of platelets were higher (p <0.05) in group 1 than in group 2 after stimulating with PAF and ADP, but not with thrombin and arachidonic acid. We concluded that the causes for the susceptibility of some hemodialysis patients to vascular access occlusion were multifactorial. In addition to previously reported plasma factors, there was a sub-group of patients who showed greater elevations of agonists stimulated platelet intracellular calcium levels.
journal_name
Thromb Haemostjournal_title
Thrombosis and haemostasisauthors
Chou KJ,Jan CR,Lee PT,Chen CL,Chung HM,Hwang YY,Chou JD,Fang HCdoi
10.1160/TH04-01-0048keywords:
subject
Has Abstractpub_date
2004-09-01 00:00:00pages
621-6issue
3eissn
0340-6245issn
2567-689Xpii
04090621journal_volume
92pub_type
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