Surface markers of platelet function in idiopathic nephrotic syndrome in children

Tkaczyk, Marcin; Baj, Zbigniew

doi:10.1007/s00467-002-0865-7

Cited by 40 publications

(35 citation statements)

References 35 publications

(49 reference statements)

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“…Sirolli et al [4] found pronounced platelet activation in nephrotic syndrome and suggested that it may contribute to the hypercoagulability of nephrosis. Increased platelet activation in nephrotic syndrome was also found by Tkaczyk and Baj [3] and Kilis-Pstrusinska et al [5]. The analysis of platelet indices revealed small volume (MPV) and differences in size (increased PDW).…”

Section: Discussionsupporting

confidence: 51%

“…Patients with heavy proteinuria, hypoalbuminemia, and hypercholesterolemia demonstrate increased concentrations of fibrinogen and C-protein, and a decreased level of antithrombin III [1,2]. There is some evidence that the platelet count (PLT) and state of platelet activation may contribute to the hypercoagulability of nephrosis [3,4,5]. Blood platelets play a crucial role in the pathogenesis of thrombotic changes in various pathological states [6,7,8,9,10,11,12].…”

Section: Introductionmentioning

confidence: 99%

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Platelet-derived growth factor and platelet profiles in childhood nephrotic syndrome

et al. 2004

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The aim of the study was to investigate (1) whether there are any changes in release of platelet-derived growth factor AA (PDGF AA) in children with nephrotic syndrome without clinical thromboembolic symptoms 2; (2) whether serum PDGF AA correlates with the platelet count (PLT) and platelet indices; (3) whether prednisone therapy affects the serum PDGF AA and the PLT; (4) whether PDGF AA is a useful predictor of disease activity. The study involved two groups of children: 33 with nephrotic syndrome (I) who were evaluated twice (A during relapse and B after 2 weeks of prednisone treatment) and 34 healthy children (II). The serum concentration of PDGF was measured by ELISA. In group I/A the PLT (P<0.01) and platelet distribution width (P<0.05) were elevated, the mean platelet volume (MPV) (P<0.05) was decreased and the plateletcrit (P>0.05) was normal. In group I/B, the PLT was decreased and MPV increased. The concentration of PDGF AA was still increased and correlated negatively with the albumin concentration. Hence in children with nephrotic syndrome an increase in PLT, a decrease in MPV, and a higher concentration of PDGF were observed. Treatment of nephrotic syndrome with prednisone for 2 weeks is not sufficient to normalize platelet parameters. Further studies are necessary to confirm the role of PDGF AA in the hypercoagulation state in children with nephrotic syndrome.

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Section: Discussionsupporting

confidence: 51%

Section: Introductionmentioning

confidence: 99%

Platelet-derived growth factor and platelet profiles in childhood nephrotic syndrome

et al. 2004

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“…We failed to identify any factors with a direct link to vWF activity in nephrotic children. As we have shown previously, the increased release of vWF in early relapse of INS might be caused by platelet activation, but in the following stages of the disease the endothelium might well become its primary source [28]. Importantly, our study does have some limitations since its results might be influenced by selection bias.…”

Section: Discussionmentioning

confidence: 67%

Markers of Endothelial Dysfunction in Children with Idiopathic Nephrotic Syndrome

Tkaczyk¹,

Czupryniak²,

Owczarek³

et al. 2007

Am J Nephrol

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Endothelial function impairment may constitute a link between nephrotic syndrome and atherosclerosis. We assessed changes in plasma thrombomodulin, von Willebrand factor and plasminogen activator inhibitor-1 at different stages of idiopathic nephrotic syndrome in children and correlated them with clinical and biochemical parameters. The study group included 132 nephrotic children (aged 2–18 years) divided into four groups, i.e. in acute phase of the disease with proteinuria, during steroid-induced remission, steroid-free remission, and in long-term, steroid-free remission. Forty-one healthy children served as controls. Plasma thrombomodulin, plasminogen activator inhibitor-1 and von Willebrand factor activity were increased in children with early nephrotic relapse. They systematically decreased in later stages of the disease but the increase in von Willebrand factor persisted in drug-free remission. These disturbances were dependent on the degree of proteinuria and serum albumin concentration. The study revealed that nephrotic children show markers of endothelial dysfunction that are dependent on the disease activity. This leads to the hypothesis that children with severe clinical course of nephrotic syndrome may be at high risk of accelerated atherogenesis.

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“…A recent study by Tkaczyk and Baj [21] found that compared with agematched healthy controls, children in the acute phase of NS have evidence of platelet activation. Although platelet activation has been associated more with the development of arterial rather than venous thrombosis, studies have also demonstrated the role of platelet activation in venous thromboembolic events [11,22].…”

Section: Discussionmentioning

confidence: 98%

Thrombotic complications in childhood-onset idiopathic membranous nephropathy

Louis

Morgenstern

Butani

2003

Pediatric Nephrology

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While the most common clinical feature of nephrotic syndrome is generalized edema, patients are at risk of developing other problems, such as bacterial infections, electrolyte abnormalities, and venous thromboses. Adults with membranous nephropathy appear to be at the greatest risk for developing thromboses, especially renal vein thrombosis. However, the same is not true for children with membranous nephropathy. A review of pediatric membranous nephropathy stated that renal vein thrombosis is unrecorded in childhood-onset membranous nephropathy. We present our experience in managing two children with idiopathic membranous nephropathy who developed venous thromboses. To our knowledge, this is the first report of pediatric patients with membranous nephropathy to develop a thromboembolic complication without evidence of predisposing factors or coagulation abnormalities. This report emphasizes the need for appropriate evaluation of patients with membranous nephropathy who develop signs and symptoms suggestive of arterial or venous occlusion in order to avoid missing this potentially life-threatening medical complication.

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Surface markers of platelet function in idiopathic nephrotic syndrome in children

Cited by 40 publications

References 35 publications

Platelet-derived growth factor and platelet profiles in childhood nephrotic syndrome

Platelet-derived growth factor and platelet profiles in childhood nephrotic syndrome

Markers of Endothelial Dysfunction in Children with Idiopathic Nephrotic Syndrome

Thrombotic complications in childhood-onset idiopathic membranous nephropathy

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