2020
DOI: 10.1055/s-0040-1708841
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Platelets in Advanced Chronic Kidney Disease: Two Sides of the Coin

Abstract: Rates of thrombosis and bleeding episodes are both increased in patients with advanced chronic kidney disease (CKD). The pathogenic mechanisms of thrombosis in these patients include platelet activation, increased formation of platelet-leukocyte conjugates, and platelet-derived microparticles, as well as effects of uremic toxins on platelets. On the other side of the coin, platelet hyporeactivity mediated by uremic toxins and anemia contributes to the increased bleeding risk in advanced CKD. Platelets also con… Show more

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Cited by 27 publications
(21 citation statements)
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“…This speculation is based on the observations that IEA is approximately 4.5 cm from the midline at the umbilicus level and has on average 3.3 branches arising from its lateral aspect [9] . In addition, our patient had advanced CKD that is usually associated with platelet dysfunction and subsequent increased risk for bleeding [10] .…”
Section: Discussionmentioning
confidence: 93%
“…This speculation is based on the observations that IEA is approximately 4.5 cm from the midline at the umbilicus level and has on average 3.3 branches arising from its lateral aspect [9] . In addition, our patient had advanced CKD that is usually associated with platelet dysfunction and subsequent increased risk for bleeding [10] .…”
Section: Discussionmentioning
confidence: 93%
“…CD62P expression and subsequent formation of platelet‐leukocyte aggregates upregulates the pro‐inflammatory function of WBCs [22]. It is worth noting that ESRD patients have higher levels of p‐selectin on the surface of PLT compared with healthy individuals, which can bind to monocytes and NEUT via p‐selectin glycoprotein ligand‐1 (PSGL‐1), and therefore platelets can directly influence leukocyte reactivity and promote leukocyte aggregation to sites of vascular injury, which in turn causes inflammation [23]. In addition, in HD patients, an increase in NEUT‐activated particles can be accompanied by an increasing number of PLT particles, possibly due to the fact that NEUT particles contain PLT‐activating factors, a mediator that may be involved in the inflammatory response [24].…”
Section: Discussionmentioning
confidence: 99%
“…Furthermore, platelets release more α -granules on stimulation, leading to increased incorporation and expression of P-selectin on the platelet surface, which, in turn, binds to PGSL-1, which is expressed on various leukocyte subsets, including neutrophils 103 . Thus, uremic platelet dysfunction not only promotes bleeding complications 104 but also immunothrombosis in CKD 105 , 106 …”
Section: Immunophenotype Of Patients With Kidney Diseasementioning
confidence: 99%