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:10.1007/bf00868741

Cited by 3 publications

(7 citation statements)

References 31 publications

Supporting

Mentioning

Contrasting

Order By: Relevance

“…The production of MDA and TXB2 by platelets following AA challenge was also increased in NS, indicating activation of the TXA2 signal transduction system [25,35,47]. TXB2 formation after stimulation with ADP and collagen was not altered in adult patients with NS [25,35], while increased TXB2 release from platelets in response to collagen was seen in children with NS [38].…”

Section: Increased Release Of Active Substancesmentioning

confidence: 75%

“…Increased levels of active substances were also found in samples of NS patients after ex vivo platelet aggregation. Platelets from pediatric NS patients released an increased amount of ATP from dense granules in response to collagen [38]. The production of MDA and TXB2 by platelets following AA challenge was also increased in NS, indicating activation of the TXA2 signal transduction system [25,35,47].…”

Section: Increased Release Of Active Substancesmentioning

confidence: 87%

“…The effect of hypercholesterolemia on platelet function in NS is not well investigated. Some studies have reported correlations between cholesterol levels and platelet aggregation in NS [23,25], but later studies did not confirm this correlation [25,29,38].…”

Section: Stimulation Of the Cox Pathwaymentioning

confidence: 90%

“…The majority of studies report increased platelet aggregability, both in adults and children in response to various agonists: ADP [24,25,32,[34][35][36][37], collagen [25,31,32,[35][36][37][38][39], AA [26,34,35] and epinephrine [40], and increased platelet agglutination after stimulation with ristocetin [41] (Table 3). However, other studies could not find increased platelet aggregability in response to collagen [24], AA [25,26,32] and ristocetin [32].…”

Section: Hyperaggregability Of Plateletsmentioning

confidence: 99%

See 3 more Smart Citations

Platelet abnormalities in nephrotic syndrome

et al. 2015

View full text Add to dashboard Cite

Nephrotic syndrome (NS) is a common kidney disease associated with a significantly increased risk of thrombotic events. Alterations in plasma levels of pro- and anti-coagulant factors are involved in the pathophysiology of venous thrombosis in NS. However, the fact that the risk of both venous and arterial thrombosis is elevated in NS points to an additional role for blood platelets. Increased platelet counts and platelet hyperactivity have been observed in nephrotic children. Platelet hyperaggregability, increased release of active substances, and elevated surface expression of activation-dependent platelet markers have been documented. The mechanisms underlying those platelet alterations are multifactorial and are probably due to changes in plasma levels of platelet-interfering proteins and lipid changes, as a consequence of nephrosis. The causal relationship between platelet alterations seen in NS and the occurrence of thromboembolic phenomena remains unclear. Moreover, the efficiency of prophylactic treatment using antiplatelet agents for the prevention of thrombotic complications in nephrotic patients is also unknown. Thus, antiplatelet medication is currently not generally recommended for routine prophylactic therapy.

show abstract

Section: Increased Release Of Active Substancesmentioning

confidence: 75%

Section: Increased Release Of Active Substancesmentioning

confidence: 87%

Section: Stimulation Of the Cox Pathwaymentioning

confidence: 90%

Section: Hyperaggregability Of Plateletsmentioning

confidence: 99%

See 2 more Smart Citations

Platelet abnormalities in nephrotic syndrome

et al. 2015

View full text Add to dashboard Cite

show abstract

“…An increased platelet count and platelet aggregation have also been suggested as causes of thromboembolism complicating INS [9,10,24,25]. Whether these processes are of primary or secondary nature is still under debate.…”

Section: Discussionmentioning

confidence: 99%

Surface markers of platelet function in idiopathic nephrotic syndrome in children

Tkaczyk

Baj²

2002

Pediatr Nephrol

View full text Add to dashboard Cite

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.

show abstract

Decreased intraplatelet Ca 2+ release and ATP secretion in pediatric nephrotic syndrome

Svetlov¹,

Moskaleva²,

Pinelis³

et al. 1999

Pediatric Nephrology

View full text Add to dashboard Cite

Platelets play an important role in the natural history of idiopathic nephrotic syndrome (NS). Although thromboembolic events are rare, the activation of circulating platelets is generally considered an important factor in the prethrombotic state in children with NS. Platelet-activating factor (PAF), a potent endogenous phospholipid mediator of inflammation, stimulates intracellular free calcium (Ca2+) mobilization, aggregation, and release reactions in platelets obtained from normal donors. Platelet-related effects of PAF in children with NS are unknown. We studied PAF-induced intracellular Ca2+ mobilization in washed platelets and ATP secretion in platelet-rich plasma in 34 children with idiopathic NS and in 7 healthy children. There was a significant decrease in ATP secretion: 0.021+/-0.011 microg/10(7) cells with 20 nM PAF and 0.089+/-0.017 microg/10(7) platelets with 200 nM PAF versus control values (0.195+/-0.004 microg/10(7) and 0.813+/-0.09 microg/10(7), respectively). Moreover, PAF-evoked increase in intracellular free Ca2+ concentration was twofold lower in NS patients than in control subjects (230.1+/-22.4 nM versus 455.6+/-15.3 nM). Also, thrombin-induced intracellular free Ca2+ mobilization was diminished in children with NS compared with the control group. Thus, contrary to expectations, a decrease of platelet reactivity in response to PAF in vitro was observed in children with idiopathic NS. We suggest that this decreased platelet reactivity may reflect a period refractory to PAF and may be considered as platelet desensitization to PAF released in vivo in children with NS.

show abstract

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

Cited by 3 publications

References 31 publications

Platelet abnormalities in nephrotic syndrome

Platelet abnormalities in nephrotic syndrome

Surface markers of platelet function in idiopathic nephrotic syndrome in children

Decreased intraplatelet Ca 2+ release and ATP secretion in pediatric nephrotic syndrome

Contact Info

Product

Resources

About