Immunosuppressive therapy regimen and platelet activation in renal transplant patients

Graff, Jochen; Klinkhardt, Ute; Harder, Sebastian; Wegert, Wolfgang; Lenz, Tomas; Scheuermann, Ernst-Heinrich; Goßmann, Jan

doi:10.1067/mcp.2002.127115

Cited by 23 publications

(39 citation statements)

References 37 publications

(45 reference statements)

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“…CyA and other immunosuppressants may modulate this effect by changing platelet function [15,16,17,18,19]. Our study did not provide sufficient data to draw any conclusions on the mechanisms of action of CyA on platelets.…”

Section: Discussioncontrasting

confidence: 57%

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Cyclosporin A does not affect platelets in children with idiopathic nephrotic syndrome

2004

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The immunosuppressive agents administered to maintain the remission of idiopathic nephrotic syndrome (INS) may have a deleterious effect on several cell types. The aim of this study was to analyze platelet activation and reactivity in children with INS treated with cyclosporin A (CyA). The study groups comprised 16 children with remission of INS induced by CyA and 16 children with glucocorticosteroid-induced remission 8 weeks from the onset of INS relapse. Fifteen healthy children served as controls. Surface expression of CD61, CD62P, and CD42b on resting and thrombin-stimulated platelets was analyzed with flow cytometry. No differences between groups were found in CD61, CD62P, and CD42b surface expression, but markers of the coagulation cascade and fibrinolysis or endothelial injury (F1+2 prothrombin fragments, tissue plasminogen activator inhibitor 1) were elevated in patients treated with CyA compared with children on steroids and healthy controls. No correlations between markers of platelet function and CyA concentration were found. We postulate that CyA administration in nephrotic patients causes an activation of thrombinogenesis but does not influence platelet activation and reactivity in INS.

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Section: Discussioncontrasting

confidence: 57%

“…Some studies in transplant patients showed either direct or indirect effects of CyA on platelet activation [15]. Direct stimulation of selected receptors by this drug or increased aggregation has been detected [16,17,18,19].…”

Section: Introductionmentioning

confidence: 99%

Cyclosporin A does not affect platelets in children with idiopathic nephrotic syndrome

2004

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“…[17,18] Raised levels of sP-selectin predict adverse thromboembolic events such as stroke and myocardial infarction. [19][20][21] Data on platelet activation among renal transplant patients are limited to a single study by Graff et al, [9] in which all renal transplant patients had enhanced platelet activation, as indicated by expression of CD62, a marker of platelet degranulation. Our results reporting markedly raised levels of soluble P-selectin in cyclosporine-treated renal transplant patients compared with those of the patients taking tacrolimus are in good agreement with the above findings.…”

Section: Discussionmentioning

confidence: 99%

“…Hypercoagulability is thought to contribute to the development and progression of atherosclerosis [2,5] and is generally attributed to combined abnormalities in platelet and coagulation-dependent hemostasis in transplanted patients. [6,7] Changes in platelet function [8,9] and fundamental classes of coagulation components, including alterations in clotting factors, fibrinogen, and clotting inhibitors, [10] as well as fibrinolytic system abnormalities [11] may play a role in the prothrombotic state observed in renal transplant patients treated with cyclosporine.…”

Section: Introductionmentioning

confidence: 99%

Effects of Immunosuppressive Drugs on Platelet Aggregation and Soluble P-Selectin Levels in Renal Transplant Patients

et al. 2009

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Background/aim. Post-transplant cardiovascular events are associated with increased morbidity and mortality after renal transplantation. Though renal transplantation eliminates cardiovascular disease risk factors by restoring renal function, it introduces new cardiovascular risks derived partly from immunosuppressive medications. In this study, to assess the effects of various immunosuppressive drugs on platelet function of renal transplant patients, we measured soluble P selectin levels (sP-selectin) and performed platelet aggregation studies in patients who have undergone renal transplantation. Methods. sP-selectin levels and platelet aggregation induced by 5 μM adenosine diphosphate (ADP), 5 μM epinephrine, 1.25 mg/mL ristocetin, and 2 μg/mL collagen were studied by whole blood platelet lumiaggregometer in 40 renal transplant patients. Patients in group 1 (n = 24) were treated with cyclosporine/mycophenolate mofetil/ methylprednisolone, and group 2 (n = 16) were treated with tacrolimus/mycophenolate mofetil/methylprednisolone. Effects were compared with those in control groups of hypertensive subjects and healthy subjects. Results. Platelet aggregation values induced by ADP, epinephrine, ristocetin, and collagen were lower in cyclosporine-treated patients than tacrolimus-treated patients, hypertensive subjects, and healthy subjects, though the difference was not statistically significant (p > 0.05). sP-selectin levels were appreciably higher in cyclosporine-treated patients, and statistically significant differences were observed compared with those of tacrolimus-treated patients (p < 0.05), hypertensive subjects (p < 0.01), and healthy subjects (p < 0.05). Conclusion. We conclude that cyclosporine-treated renal transplant patients show enhanced platelet activation in which anti-platelet therapy should be considered, in addition to management of other conventional cardiovascular risk factors, to decrease the cardiovascular morbidity and mortality in this high risk population.

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“…Other anticoagulants, such as sodium citrate or heparin, do not affect GPIIb-IIIa, and therefore do not lead to platelet agglutination in these cases [13]. Enhanced platelet activation and subsequent aggregation has been reported in post renal transplant patients especially those on Cyclosporine and/or Azathioprine therapy [14]. Our patient was also on Cyclosporine and Azathioprine and the persistent platelet clumps even when repeat samples were drawn in heparin and sodium citrate can be possibly attributed to the effect of these drugs.…”

Section: Discussionmentioning

confidence: 98%

Co-existent Platelet Phagocytosis, Satellitism and Clumping Causing Spurious Thrombocytopenia

Paul

Kaur

Kakkar

et al. 2012

Indian J Hematol Blood Transfus

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Immunosuppressive therapy regimen and platelet activation in renal transplant patients

Cited by 23 publications

References 37 publications

Cyclosporin A does not affect platelets in children with idiopathic nephrotic syndrome

Cyclosporin A does not affect platelets in children with idiopathic nephrotic syndrome

Effects of Immunosuppressive Drugs on Platelet Aggregation and Soluble P-Selectin Levels in Renal Transplant Patients

Co-existent Platelet Phagocytosis, Satellitism and Clumping Causing Spurious Thrombocytopenia

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