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Published on: May 6, 2018
[Platelet activation in relapse idiopathic nephrotic syndrome in children]
1Klinika Nefrologii i Dializoterapii, Instytutu Centrum Zdrowia Matki Polki. mtkaczyk@krysia.uni.lodz.pl
Insights
Platelet activation is increased in children with idiopathic nephrotic syndrome (INS) relapses, posing a risk for blood clots. This activation, marked by aggregates and microparticles, decreases with early treatment.
Area of Science:
- Pediatric Nephrology
- Hematology
- Thrombosis Research
Background:
- The role of platelets in pediatric idiopathic nephrotic syndrome (INS) pathogenesis and thromboembolic complications is not fully understood.
- Platelet activation is a potential factor in the development of complications associated with INS relapses.
Purpose of the Study:
- To analyze platelet activation in whole blood during the initial 8 weeks of idiopathic nephrotic syndrome (INS) in children.
- To investigate markers of platelet activation and their correlation with clinical parameters during INS relapses.
Main Methods:
- Assessed platelet aggregates, microparticles, and surface markers (CD62P, CD42b) in 24 children with INS relapses and 16 healthy children.
- Evaluated activation markers at the onset of INS and after 2 weeks of therapy.
- Compared results between the INS patient group and the healthy control group.
Main Results:
- Increased counts of platelet aggregates and microparticles were observed at the onset of INS.
- A systematic decrease in these markers was noted within the first 2 weeks of therapy.
- Significantly lower expression of CD42b was found at the beginning of treatment, with no clear correlation to biochemical parameters.
Conclusions:
- Increased blood platelet activation is an independent risk factor for thromboembolic complications in the early stages of INS relapse.
- The precise role of platelets in the pathogenesis or induction of INS relapses requires further investigation.
Abstract:
The role that platelets play in pathogenesis and thromboembolic complications of the idiopathic nephrotic syndrome (INS) in children still remains unclear. The aim of the study was to analyse of platelet activation in whole blood during first 8 weeks of ins. Study group comprised 24 children with 34 relapses of INS by ISKDC (group A). Obtained results were compared to 16 healthy children (group B). We assessed activation by the count of platelet aggregates, microparticles and surface expression of selected markers--CD62P (P-selectin), CD42b (part of von Willebrand factor receptor) at the onset INS, after 2 weeks of therapy. We found the increased counts of platelet aggregates and microparticles at the onset of INS with a systematic decrease in following 2 weeks. Furthermore, expression of CD42b was significantly lower at the beginning of therapy. There were no clear correlation between markers of activation and biochemical parameters in the study group. According to these findings we conclude that increased activation of blood platelets is an independent risk factor of thromboembolic complication in the early stages of relapse of INS. The role of platelets in pathogenesis or induction of ins relapse remains the matter for further investigation.
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