title: Platelet hyperreactivity in hemodialysis patients with frequently occluded vascular access.
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.
authors.affiliation: Division of Nephrology, Department of Internal Medicine, Kaohsiung Veterans General Hospital, 386 Ta-Chung 1 st Rd, Kaohsiung, Taiwan 813.
authors.forename: Kang-Ju
authors.initials: KJ
authors.lastname: Chou
authors.forename: Chung-Ren
authors.initials: CR
authors.lastname: Jan
authors.forename: Po-Tsang
authors.initials: PT
authors.lastname: Lee
authors.forename: Chien-Liang
authors.initials: CL
authors.lastname: Chen
authors.forename: Hsiao-Min
authors.initials: HM
authors.lastname: Chung
authors.forename: Yueh-Yen
authors.initials: YY
authors.lastname: Hwang
authors.forename: Jing-Dung
authors.initials: JD
authors.lastname: Chou
authors.forename: Hua-Chang
authors.initials: HC
authors.lastname: Fang
mesh_terms: D000244:Adenosine Diphosphate / Q000494:pharmacology; D016718:Arachidonic Acid / Q000494:pharmacology; D002118:Calcium / Q000378:metabolism; D002408:Catheters, Indwelling / Q000009:adverse effects*; D003920:Diabetes Mellitus / Q000097:blood / Q000628:therapy; D005260:Female; D006083:Graft Occlusion, Vascular / Q000097:blood*; D006801:Humans; D008297:Male; D008875:Middle Aged; D010972:Platelet Activating Factor / Q000494:pharmacology; D015539:Platelet Activation; D006435:Renal Dialysis / Q000009:adverse effects*; D013917:Thrombin / Q000494:pharmacology; D013927:Thrombosis / Q000209:etiology
chemical_list: D010972:Platelet Activating Factor; D016718:Arachidonic Acid; D000244:Adenosine Diphosphate; D013917:Thrombin; D002118:Calcium