Abstract Number: PB1474
Meeting: ISTH 2020 Congress
Background: Patients with chronic kidney disease (CKD) are at high risk for thrombotic and cardiovascular complications. Counterintuitively, CKD patients also present with an increased risk of bleeding. Multiple platelet defects have been described, but data are conflicting.
Aims: To better understand the etiology of the altered platelet phenotype in CKD.
Methods: After written informed consent, blood was drawn from 29 patients with CKD stages 3-5 as approved by the local medical ethics committee. In case of hemodialysis (HD), blood was drawn prior to HD. Patients on anticoagulant or antiplatelet therapy were excluded from participation except for CKD5HD patients treated with 100 mg aspirin. Blood from healthy volunteers served as control. Platelet activation was measured using flow cytometry. Thrombus formation on a collagen type I surface under flow was used to assess the hemostatic potential.
Results: In total, we included 13 CKD3, 6 CKD4, and 10 CKD5HD patients (of whom 5 were on aspirin). Only CKD5HD patients without aspirin exhibited a reduced platelet count (p=0.013 vs. healthy controls). Platelet counts of CKD5HD patients on aspirin were comparable to those of healthy controls and were increased compared to HD patients not on aspirin (p=0.044). Platelet activation (integrin αIIbβ3 activation, P-selectin expression) upon collagen-related peptide was mildly decreased in all CKD groups. ADP and TRAP induced activation was comparable to that of healthy controls. Thrombus formation on collagen under flow was impaired in CKD4, CKD5HD and CKD5HD patients on aspirin, although thrombus formation in CKD5HD with aspirin was increased compared to CKD5HD (p=0.0033). Furthermore, platelet adhesion and aggregation under flow showed a significant correlation to glomerular filtration rate as a read-out of kidney function in CKD patients not receiving HD
(r=0.6276 and 0.5896, respectively).
Conclusions: Platelet function impairment in CKD correlates with disease severity and is likely a consequence of pre-activation of circulating platelets resulting in secondary exhaustion.
To cite this abstract in AMA style:Baaten C, Sternkopf M, Stamellou E, Saritas T, Jankowski J, Floege J, Noels H. Uremia Induced Pre-Activation Results in Platelet Function Impairment in Chronic Kidney Disease [abstract]. Res Pract Thromb Haemost. 2020; 4 (Suppl 1). https://abstracts.isth.org/abstract/uremia-induced-pre-activation-results-in-platelet-function-impairment-in-chronic-kidney-disease/. Accessed October 1, 2023.
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