Laser aggregometer studies, ATP release and thromboxane B2 release and cAMP concentration of the platelets in nephrotic syndrome

Túri, Sándor; Bereczki, Cs.; Torday, Csilla; Havass, Z

doi:10.1016/0952-3278(94)90181-3

Cited by 6 publications

(7 citation statements)

References 16 publications

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“…73 The platelet sensitivity was not completely nor malized during remission. This last study seems to be concordant with the results of Turi et al 68 and suggests the use of multiple doses of arachidonic acid in aggregometric studies.…”

Section: Platelet Abnormalitiessupporting

confidence: 91%

“…65,[69][70][71][72] Recently, a pediatric study, involving 56 children with NS, has shown that the increased platelet aggregation observed during flare-ups might be prolonged in early remission (<6 months). 68 More re cently, a higher sensitivity of platelets to low doses of arachidonic acid was found during relapse of childhood NS. 73 The platelet sensitivity was not completely nor malized during remission.…”

Section: Platelet Abnormalitiesmentioning

confidence: 98%

“…Alterations in platelet function have been reported in a number of publications. Enhanced platelet aggregability has been demonstrated by many authors in adults [15][16][17][61][62][63][64][65][66][67][68][69][70] and in children. [67][68][69][70] This hyperaggregability has been observed in the presence of different in ducers such as ADP, collagen, arachidonic acid, and thrombin.…”

Section: Platelet Abnormalitiesmentioning

confidence: 99%

“…Enhanced platelet aggregability has been demonstrated by many authors in adults [15][16][17][61][62][63][64][65][66][67][68][69][70] and in children. [67][68][69][70] This hyperaggregability has been observed in the presence of different in ducers such as ADP, collagen, arachidonic acid, and thrombin. 65,[69][70][71][72] Recently, a pediatric study, involving 56 children with NS, has shown that the increased platelet aggregation observed during flare-ups might be prolonged in early remission (<6 months).…”

Section: Platelet Abnormalitiesmentioning

confidence: 99%

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Thromboembolic Risks and Complications in Nephrotic Children

Schlegel

1997

Semin Thromb Hemost

103

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The identification of many biologic anomalies is progressively realized in nephrotic children, thanks to adult studies and to scientific advances. The number of anomalies and the intensity of alterations vary from one patient to another and during flare-ups in the same patient. Their severity is usually a function of the severity of the nephrotic syndrome (NS). The responsibility of each anomaly per se in triggering thrombotic complications is not yet known and today it is understood that the coexistence of several factors is necessary to induce these complications. Thus, the NS presents a true model because it can gather multiple thrombogenic anomalies. It might be more satisfying to characterize all of the mechanisms that could be responsible for a thrombosis rather than to assay all of the biologic components in one patient. When the main balances during the childhood NS are broken-pro- versus anticoagulant forces, pro- versus antifibrinolytic forces, platelet/vessel wall interactions-one cannot evaluate with accuracy the possible impact of acquired interrelations such as a decrease of antithrombin versus an increase of protein C. Among the present unknown factors, a major one is related to the effects, if any, of the proteinuric factor (recently discovered) on the vascular endothelium and the central question is: would it be capable of changing the thromboresistant phenotype to a thrombogenic one? No absolute correlation has been found between the many biologic abnormalities and the occurrence of thromboembolic (TE) complications. However, it is of great interest to have the best evaluation of the TE risks in nephrotic children. The criteria that are commonly used are: albuminuria, and plasma levels of fibrinogen and antithrombin. One can suggest adding to these criteria the D-dimer assay, a molecular marker of coagulation activation, and the factor V Leiden workup because it represents a genetic predisposition for TE complications. As far as prevention of TE complications is concerned, the standard but basic guidelines of nephrotic patients must be followed. Furthermore, vitamin K antagonists should be administered as soon as the risk criteria are gathered, but only after a careful evaluation of the benefits/risks ratio. As to the treatment of TE events, one should follow the present recommendations for children. A better future regarding prevention of TE accidents is based not only on the necessity of multicentric prospective studies but also on basic research that will allow discovery of the "primum movens" of childhood NS.

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Section: Platelet Abnormalitiessupporting

confidence: 91%

Section: Platelet Abnormalitiesmentioning

confidence: 98%

Section: Platelet Abnormalitiesmentioning

confidence: 99%

Section: Platelet Abnormalitiesmentioning

confidence: 99%

See 2 more Smart Citations

Thromboembolic Risks and Complications in Nephrotic Children

Schlegel

1997

Semin Thromb Hemost

103

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“…However, the role of platelet function in nephrosis is controversial. 26 Turi et al 27 reported the finding on the platelet function in children with different forms of NS. There were increases in platelet aggregation, thromboxane release, and cAMP concentration in the platelets, concluding that increased platelet activation may play a role in the pathogenesis of NS.…”

Section: Discussionmentioning

confidence: 99%

Relationship of serum interleukin‐7 concentration and the coagulation state in children with nephrotic syndrome

Wasilewska

Zoch-Zwierz

Tomaszewska

et al. 2005

Pediatrics International

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Surface markers of platelet function in idiopathic nephrotic syndrome in children

Tkaczyk

Baj²

2002

Pediatr Nephrol

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The objective of the study was to investigate platelet activation markers in whole blood in idiopathic nephrotic syndrome (INS) in children. The study group consisted of 34 children with 45 relapses of INS, 35 children in long-term remission of INS, and 26 healthy controls. Using flow cytometry we measured the percentage of platelet microparticles, platelet-platelet aggregates, and surface expression of CD62P (P-selectin) and CD42b (a component of von Willebrand factor receptor). We found an increased percentage of microparticles and platelet-platelet aggregates, decreased expression of CD42b in the first 2 weeks of INS relapse. CD62P expression was elevated only at the onset of INS relapse when compared with the long-term remission group and healthy subjects. Children in long-term INS remission did not differ from healthy controls. There was no significant correlation between platelet activation markers and selected biochemical factors of blood in children with INS. Activation of the coagulation cascade was confirmed by an elevated serum concentration of F1+2 prothrombin fragment during follow-up. These findings suggest that platelets may contribute independently to the prothrombotic state in the early stages of INS, but their role in triggering relapses remains to be investigated.

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Laser aggregometer studies, ATP release and thromboxane B2 release and cAMP concentration of the platelets in nephrotic syndrome

Cited by 6 publications

References 16 publications

Thromboembolic Risks and Complications in Nephrotic Children

Thromboembolic Risks and Complications in Nephrotic Children

Relationship of serum interleukin‐7 concentration and the coagulation state in children with nephrotic syndrome

Surface markers of platelet function in idiopathic nephrotic syndrome in children

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