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

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 gro...

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Bibliographic Details
Published in:Pediatric nephrology (Berlin, West) West), 2005-01, Vol.20 (1), p.30-35
Main Authors: Tkaczyk, Marcin, Baj, Zbigniew, Nowicki, Michał
Format: Article
Language:English
Subjects:
Adolescent
Atherosclerosis
Biomarkers - blood
Blood Platelet Disorders - chemically induced
Blood platelets
Blood Platelets - drug effects
Blood pressure
Care and treatment
Child
Child, Preschool
Complications and side effects
Cross-Sectional Studies
Cyclosporine
Cyclosporine - adverse effects
Drug dosages
Female
Flow Cytometry
Humans
Immunosuppressive Agents - adverse effects
Integrin beta3 - blood
Kidney diseases
Male
Nephrotic syndrome
Nephrotic Syndrome - drug therapy
P-Selectin - blood
Platelet Activation - drug effects
Platelet Glycoprotein GPIb-IX Complex - analysis
Steroids
Thrombosis
Transplants & implants
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Summary: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.
ISSN:0931-041X
1432-198X
DOI:10.1007/s00467-004-1674-y