In vivo platelet activity and serum albumin concentration in nephrotic syndrome

Goubran, F.; Maklady, Fathi A.

doi:10.1007/bf00320629

Cited by 7 publications

(5 citation statements)

References 13 publications

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“…The mechanism of PLT increase in nephrotic syndrome is unknown. It is assumed that biochemical disorders associated with hypoalbuminemia and hypercholesterolemia lead to increased platelet aggregation and are responsible for the elevated PLT [7,26,27,28,29]. Our study has confirmed these observations only with reference to albumin concentration-we found a negative linear correlation between PLT and albumin.…”

Section: Discussionsupporting

confidence: 91%

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: 91%

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

et al. 2004

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“…The relationship between albuminemia and platelet activation markers was further studied. An inverse correlation between serum albumin levels and platelet aggregation, both spontaneous and in response to various aggregation inducers, was found in some studies [23,25,26,39,52], but was not confirmed in others [25,31,35,53].2 Inverse correlations were also observed between serum albumin levels and several markers of platelet activation, such as β-thromboglobulin levels [43,52], PDGF [30], TXB2 generation in response to AA [35] and platelet adhesiveness [23]. Stuart et al found that the net conversion to TXB2 was not dependent on albumin concentration in normal platelets [40].…”

Section: Stimulation Of the Cox Pathwaymentioning

confidence: 68%

“…Several substances released from α-granules upon platelet activation were elevated in plasma during NS. β-thromboglobulin, a platelet-specific protein, was repeatedly found to be elevated in adults during NS [23,25,37,42,43]. Platelet-derived growth factor (PDGF) [30] and interleukin-7 (IL-7) [44] were increased in pediatric patients during NS, while plasma levels of platelet factor 4, another α-granule component, were normal [23,25].…”

Section: Increased Release Of Active Substancesmentioning

confidence: 97%

Platelet abnormalities in nephrotic syndrome

et al. 2015

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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.

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“…Thus, the increase of BTG excretion even then sur passes the retention coming from the decreas ing BTG catabolism. So, the rising of the plasma BTG level would also in end-stage renal disease partly reflect an in vivo hyperac tivation of the platelets [35,36].…”

Section: Discussionmentioning

confidence: 99%

Elevated Levels of Plasma and Urine Beta-Thromboglobulin or Thromboxane-B<sub>2</sub> as Markers of Real Platelet Hyperactivation in Diabetic Nephropathy

Tóth

Szénási

Varsányi

et al. 1992

Pathophysiol Haemos Thromb

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Serum creatinine, immunoreactive serum and urine β₂-microglobulin, plasma and urine thromboglobulin, plasma thromboxane-B₂ levels and daily protein excretion were determined in 61 insulin-treated diabetic patients, comparing the different patient groups (complication free, nephropathy without and with azotaemia) with control subjects. In the groups of diabetic patients, plasma and urine β-thromboglobulin (BTG) and plasma thromboxane-B₂ levels were higher than in the controls. There was a significant positive correlation between urine BTG and β₂-microglobulin in the group without complication, and between the plasma BTG and β₂-microglobulin, and plasma BTG and thromboxane levels in the diabetic group with azotaemia. In contrast to some previous assumptions, the increased level of plasma BTG reflects a real platelet hyperactivation in patients with diabetic nephropathy. At the same time, urine BTG also increases. Determination of urine BTG is more simple with less possibility of methodological error.

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In vivo platelet activity and serum albumin concentration in nephrotic syndrome

Cited by 7 publications

References 13 publications

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

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

Platelet abnormalities in nephrotic syndrome

Elevated Levels of Plasma and Urine Beta-Thromboglobulin or Thromboxane-B<sub>2</sub> as Markers of Real Platelet Hyperactivation in Diabetic Nephropathy

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