Thromb Haemost 2004; 92(03): 621-626
DOI: 10.1160/TH04-01-0048
Platelets and Blood Cells
Schattauer GmbH

Platelet hyperreactivity in hemodialysis patients with frequently occluded vascular access

Kang-Ju Chou
1   Division of Nephrology, Department of Internal Medicine, Kaohsiung Veterans General Hospital, Kaohsiung, Taiwan
2   National Yang-Ming University, School of Medicine, Taipei, Taiwan
,
Chung-Ren Jan
3   Department of Medical Education and Research, Kaohsiung Veterans General Hospital, Kaohsiung Taiwan
,
Po-Tsang Lee
1   Division of Nephrology, Department of Internal Medicine, Kaohsiung Veterans General Hospital, Kaohsiung, Taiwan
2   National Yang-Ming University, School of Medicine, Taipei, Taiwan
,
Chien-Liang Chen
1   Division of Nephrology, Department of Internal Medicine, Kaohsiung Veterans General Hospital, Kaohsiung, Taiwan
2   National Yang-Ming University, School of Medicine, Taipei, Taiwan
,
Hsiao-Min Chung
1   Division of Nephrology, Department of Internal Medicine, Kaohsiung Veterans General Hospital, Kaohsiung, Taiwan
2   National Yang-Ming University, School of Medicine, Taipei, Taiwan
,
Yueh-Yen Hwang
1   Division of Nephrology, Department of Internal Medicine, Kaohsiung Veterans General Hospital, Kaohsiung, Taiwan
,
Jing-Dung Chou
1   Division of Nephrology, Department of Internal Medicine, Kaohsiung Veterans General Hospital, Kaohsiung, Taiwan
,
Hua-Chang Fang
1   Division of Nephrology, Department of Internal Medicine, Kaohsiung Veterans General Hospital, Kaohsiung, Taiwan
2   National Yang-Ming University, School of Medicine, Taipei, Taiwan
› Institutsangaben
Financial support: This work was supported by grants from the National Science Council (NSC89-2320-B-075B-015) and Kaohsiung Veterans General Hospital (VGHKS91-46) to Dr. Kang-Ju Chou and (VGHKS91-47) to Dr. Hua-Chang Fang.
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Publikationsverlauf

Received 26. Januar 2004

Accepted after revision 09. Mai 2004

Publikationsdatum:
30. November 2017 (online)

Summary

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 Ca2+ levels ([Ca2+]i) leading to aggregation and thrombosis. We compared the platelet [Ca2+]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 [Ca2+]i after stimulation with 1 U/ml thrombin, 1 µM arachidonic acid, 1 µM platelet activation factor (PAF), and 10 µM adenosine diphosphate (ADP), respectively. Our results showed that in Ca2+-containing media, there was no significant differences in the basal [Ca2+]i , but the maximal increases of [Ca2+]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 subgroup of patients who showed greater elevations of agonists stimulated platelet intracellular calcium levels.

 
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