Uremic toxins and platelet function

1970 ◽  
Vol 126 (5) ◽  
pp. 823-826 ◽  
Author(s):  
H. I. Horowitz
2021 ◽  
pp. ASN.2020101440
Author(s):  
Constance C.F.M.J. Baaten ◽  
Marieke Sternkopf ◽  
Tobias Henning ◽  
Nikolaus Marx ◽  
Joachim Jankowski ◽  
...  

BackgroundPatients with CKD are at high risk for thrombotic and hemorrhagic complications. Abnormalities in platelet function are central to these complications, but reports on platelet function in relation to CKD are conflicting, and vary from decreased platelet reactivity to normal or increased platelet responsiveness. The direct effects of uremic toxins on platelet function have been described, with variable findings.MethodsTo help clarify how CKD affects platelet function, we conducted a systematic review and meta-analysis of platelet activity in CKD, with a focus on nondialysis-induced effects. We also performed an extensive literature search for the effects of individual uremic toxins on platelet function.ResultsWe included 73 studies in the systematic review to assess CKD’s overall effect on platelet function in patients; 11 of them described CKD’s effect on ex vivo platelet aggregation and were included in the meta-analysis. Although findings on platelet abnormalities in CKD are inconsistent, bleeding time was mostly prolonged and platelet adhesion mainly reduced. Also, the meta-analysis revealed maximal platelet aggregation was significantly reduced in patients with CKD upon collagen stimulation. We also found that relatively few uremic toxins have been examined for direct effects on platelets ex vivo; ex vivo analyses had varying methods and results, revealing both platelet-stimulatory and inhibitory effects. However, eight of the 12 uremic toxins tested in animal models mostly induced prothrombotic effects.ConclusionsOverall, most studies report impaired function of platelets from patients with CKD. Still, a substantial number of studies find platelet function to be unchanged or even enhanced. Further investigation of platelet reactivity in CKD, especially during different CKD stages, is warranted.


1970 ◽  
Vol 126 (5) ◽  
pp. 823 ◽  
Author(s):  
Herbert I. Horowitz

Author(s):  
W.T. Gunning ◽  
J.N. Turner ◽  
K. Buttle ◽  
E.P. Calomeni ◽  
N.A. Lachant ◽  
...  

There are a variety of conditions which have been associated with prolonged bleeding times. If other etiologies including von Willebrand's disease have been ruled out, a platelet function disorder must be considered. The best, if not only, technique to make this diagnosis is the electron microscopic evaluation of whole air dried platelets. Bull first described the presence of dense granules in whole platelets in 1968 and the technique has been utilized extensively The electron dense or delta granules are easily distinguished from the larger more numerous alpha granules which are electron lucent. The significance of the dense granules is that they are known to be “storage pools” of serotonin, calcium, adenosine di- and triphosphate, and pyrophosphate. Prolonged bleeding times may be directly related to an insufficiency of these substances. The diagnosis of a storage pool deficiency is made when either the storage content of the dense granules is abnormal or their number is diminished. We observe normal platelets to have 4-6 dense granules, which agrees with the literature.


1970 ◽  
Vol 126 (5) ◽  
pp. 843-845 ◽  
Author(s):  
P. L. Balestri
Keyword(s):  

VASA ◽  
2011 ◽  
Vol 40 (6) ◽  
pp. 429-438 ◽  
Author(s):  
Berent ◽  
Sinzinger

Based upon various platelet function tests and the fact that patients experience vascular events despite taking acetylsalicylic acid (ASA or aspirin), it has been suggested that patients may become resistant to the action of this pharmacological compound. However, the term “aspirin resistance” was created almost two decades ago but is still not defined. Platelet function tests are not standardized, providing conflicting information and cut-off values are arbitrarily set. Intertest comparison reveals low agreement. Even point of care tests have been introduced before appropriate validation. Inflammation may activate platelets, co-medication(s) may interfere significantly with aspirin action on platelets. Platelet function and Cox-inhibition are only some of the effects of aspirin on haemostatic regulation. One single test is not reliable to identify an altered response. Therefore, it may be more appropriate to speak about “treatment failure” to aspirin therapy than using the term “aspirin resistance”. There is no evidence based justification from either the laboratory or the clinical point of view for platelet function testing in patients taking aspirin as well as from an economic standpoint. Until evidence based data from controlled studies will be available the term “aspirin resistance” should not be further used. A more robust monitoring of factors resulting in cardiovascular events such as inflammation is recommended.


1975 ◽  
Vol 33 (01) ◽  
pp. 063-065 ◽  
Author(s):  
Marjorie B Zucker
Keyword(s):  

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