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Atherosclerotic and hemostatic abnormalities in patients undergoing hemodialysis
Fumihiko Kushiya1, Hideo Wada, Miho Sakakura
1Second Department of Internal Medicine, Mie University School of Medicine, Tsu-City, Mie-ken, Japan.
Insights
Patients on hemodialysis (HD) show progressive atherosclerosis linked to hemostatic abnormalities. Prolonged HD worsens atherosclerosis markers and alters blood clotting factors, increasing vascular event risks.
Area of Science:
- Cardiovascular Medicine
- Nephrology
- Hematology
Background:
- Atherosclerosis is a primary cause of death in hemodialysis (HD) patients.
- Understanding the link between atherosclerosis and hemostasis in HD is crucial for risk stratification.
Purpose of the Study:
- To investigate the relationship between atherosclerosis indicators and hemostatic markers in hemodialysis patients.
- To assess the impact of hemodialysis duration on atherosclerosis and hemostasis.
Main Methods:
- Evaluated 84 hemodialysis patients using Fontaine score, ankle blood pressures, and aortic calcification index (ACI).
- Assessed plasma levels of fibrinogen, PIC, TM, D-dimer, PC, AT, TAT, and tPA-PAI-1 complex.
- Correlated atherosclerosis tests and hemostatic markers with hemodialysis duration and ankle-brachial index (ABI).
Main Results:
- High prevalence of atherosclerosis (66% Fontaine, 33% ankle BP, 79% ACI).
- Prolonged HD increased Fontaine score and ACI; decreased ABI with >10 years HD.
- Significant alterations in hemostatic markers observed, including increased D-dimer and TAT, and decreased PC and AT with prolonged HD.
Conclusions:
- Hemodialysis patients exhibit progressive atherosclerosis.
- Hemostatic abnormalities are associated with atherosclerosis in HD patients.
- Findings suggest a link between HD duration, atherosclerosis progression, and altered coagulation.
Abstract:
Vascular events caused by atherosclerosis are the major cause of death in patients undergoing hemodialysis (HD). The relationship between the tests of atherosclerosis and hemostasis in 84 patients with HD was examined. Abnormal test results indicting the occurrence of atherosclerosis were found in 66% by the Fontaine score, in 33% by ankle blood pressures, and in 79% by aortic calcification index (ACI). When HD was prolonged, the mean Fontaine score and ACI were further increased. Particularly, the ACI tended to correlate with HD duration. The ankle-brachial index (ABI) was decreased in patients with HD duration of more than 10 years. Before HD, the plasma levels of fibrinogen, plasmin-plasmin inhibitor complex (PIC), thrombomodulin (TM), and D-dimer were increased, while the plasma levels of protein C (PC), antithrombin (AT), thrombin-antithrombin complex (TAT), and tissue plasminogen activator (tPA)-plasminogen activator inhibitor-I (PAI-I) complex (tPA-PAI-1 complex) were decreased. With prolonged HD, the plasma levels of AT and PC were decreased, while those of D-dimer were increased. The plasma levels of TAT and TPA-PAI-1 complex were significantly increased and those of PIC, soluble fibrin (SF) and D-dimer tended to be high in patients with less than 0.7 of ABI. The plasma levels of D-dimer, TPA-PAI-1 complex, TAT, PIC, and SF tended to be high in patients with more than 0.5 in ABI. These findings suggest that patients undergoing HD have progressive atherosclerosis and that this is associated with some hemostatic abnormalities.
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