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Open AccessJournal ArticleDOI

Impaired expression of glycoproteins on resting and stimulated platelets in uraemic patients

TLDR
Findings indicate that uraemic platelets are hyporesponsive to stimulation, compared with controls, which indicates that chronic renal failure patients with CRF are likely to have low platelet function.
Abstract
Background. The increased bleeding tendency of chronic renal failure (CRF) patients has been attributed to platelet dysfunction. However, reports on various platelet functions in uraemic patients have been conflicting. The present study sought to analyse platelet function by examining their surface glycoproteins in well-identified populations ofCRF patients. Methods. Three groups were studied: 22 chronic haemodialysis (HD) patients, 25 conservatively treated patients with CRF and 30 controls. Bleeding tendency was assessed by measuring bleeding time and by recording current haemorrhagic symptoms. We measured the fibrinogen receptor GPIIbIIIa, the von Willebrand receptor GPIb, and P-selectin levels on the platelet surface using flow cytometry. Results. Forty percent ofCRF and 45% ofHD patients had bleeding. The bleeding time was similar in the HD and CRF groups, but was longer in both groups than in controls. In resting platelets, GPIb expression was lower in CRF patients than in controls. In stimulated platelets (i) GPIb expression was higher in HD patients than in both controls and CRF patients; and (ii) GPIIbIIIa and P-selectin expression were lower in CRF and HD patients than in controls. Conclusions. These findings indicate that uraemic platelets are hyporesponsive to stimulation.

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Direct oral anticoagulants in patients with chronic kidney disease: patient selection and special considerations.

TL;DR: In patients with an estimated glomerular filtration rate (eGFR) above 60 mL/min, DOACs can be used safely with greater efficacy and safety as compared to VKAs, and in patients with impaired renal function, they are as effective as VKAs with a lower bleeding rate.
References
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Journal ArticleDOI

A platelet alpha-granule membrane protein (GMP-140) is expressed on the plasma membrane after activation.

TL;DR: It is demonstrated that GMP-140 is an alpha-granule membrane protein that is expressed on the platelet plasma membrane during degranulation.
Journal ArticleDOI

Thrombin induces a rapid redistribution of glycoprotein Ib-IX complexes within the membrane systems of activated human platelets

TL;DR: An increased presence of GP Ib-IX complexes within surface-connected membrane systems of the thrombin-stimulated platelets was confirmed and movement was opposite to the thROMbin-induced externalization of internal pools of GP IIb- IIIa complexes and of the alpha-granule membrane GP, GMP-140.
Journal ArticleDOI

Thrombin-induced changes in platelet membrane glycoproteins Ib, IX, and IIb-IIIa complex.

TL;DR: Thrombin-induced changes in platelet membrane glycoprotein Ib and the GPIIb-IIIa complex may be important in modulating the reactivity of platelets with the damaged vessel wall and with each other.
Journal ArticleDOI

Hemostatic disorder of uremia : The platelet defect, main determinant of the prolonged bleeding time, is correlated with indices of activation of coagulation and fibrinolysis

TL;DR: Links between primary hemostasis and activation of coagulation and fibrinolysis suggest that increased intravascular generation of thrombin and/or plasmin is an important mediator of the defects in primary he mostasis, prolongation of the BT and, probably, bleeding in CRF.
Journal ArticleDOI

Plasma and platelet von Willebrand factor defects in uremia

TL;DR: The data suggest that the uremic platelet-binding sites for von Willebrand factor are intact and that the defect in ristocetin-induced platelet aggregation is most likely plasmatic in nature.
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These findings indicate that uraemic platelets are hyporesponsive to stimulation.