Platelet hyperaggregability as a consequence of the nephrotic syndrome

Walter, E.; Deppermann, D.; Andrássy, K.; Koderisch, J.

doi:10.1016/0049-3848(81)90171-7

Cited by 26 publications

(23 citation statements)

References 14 publications

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“…In 1981, Walter et al reported for the first time a statistically significant increased mean PLT count of 281×10 9 /l in adult patients with NS in comparison to 216×10 9 /l in the healthy control group [23]. This was later confirmed by two studies [24,25], while other studies found a normal PLT count in adult patients with NS [26,27].…”

Section: Changes In Platelet Count and Morphology During Nephrotic Symentioning

confidence: 87%

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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Section: Changes In Platelet Count and Morphology During Nephrotic Symentioning

confidence: 87%

Platelet abnormalities in nephrotic syndrome

et al. 2015

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“…Previous reports on nephrotic patients suggested that the enhanced aggregation responses to ADP [11,20,24] and arachidonic acid [5] were the result of reduced albumin concentration. However, not all patients with reduced albumin levels in our study showed enhanced aggregation and vice versa; in fact the mean albumin level of patients in some clinical groups showing normal responses to ADP was slightly lower than the mean albumin level in those showing enhanced responses.…”

Section: Discussionmentioning

confidence: 99%

Haemostatic measurements in childhood nephrotic syndrome

et al. 1991

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Blood coagulation and platelet aggregation were assessed in children with nephrotic syndrome who were divided into the following groups: (1) relapse without treatment: (2) relapse on steroids; (3) early remission; (4) late remission and (5) steroid resistant. The renal histological findings were also recorded. Plasma anti-thrombin III (ATIII) levels were markedly reduced in groups 1 and 2, below normal in group 3 and were normal in groups 4 and 5. There was significant urinary loss of ATIII in groups 1 and 2 as well as in group 5. Plasma fibrinogen fluctuations exhibited the expected negative correlations with plasma ATIII. Reptilase time showed significant prolongation in groups 1, 2 and 3, and was near normal in groups 4 and 5. Platelet aggregation in response to arachidonic acid exhibited aggregation followed by disaggregation in groups 1, 2, 4 and 5, and was normal in group 3. Hyperaggregation in response to decreasing doses of ADP was noted in all patient groups as well as controls with no relationship to serum albumin levels. Aggregation responses to collagen and ristocetin were normal. It is concluded that: 1. The fluctuations in ATIII levels in childhood nephrotic syndrome are determined by the response to steroids and not by the renal histology per se. 2. An acquired fibrin polymerization defect (dysfibrinogenaemia) and an abnormality of the prostaglandin pathway of platelet activation, both reversible, are yet other haemostatic abnormalities in childhood nephrosis. 3. The discrepancies in the literature on haemostatic parameters, specially ATIII in childhood nephrosis, would not have arisen if their fluctuation in relation to steroid therapy as well as the renal histological features of nephrotic syndrome had been documented simultaneously.

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“…The true incidence of in creased platelet release in vivo in our patients was ob scured by the presence of reduced renal function or evidence for in vitro platelet release (high platelet factor4 levels) in the majority of patients studied. These limita tions must be kept in mind when interpreting the findings of other studies [9][10][11], especially when platelet factor 4 levels are not reported.…”

Section: Discussionmentioning

confidence: 99%

“…Increased levels of fibrinogen and other procoagulants [1][2][3], decreased antithrom bin III and plasminogen levels [4][5][6][7][8], and increased plate let aggregability [9][10][11] have been considered the major contributing factors to thrombosis. However, not all pa tients with significant abnormalities of platelets, pro coagulants, antithrombin III, or the fibrinolytic system develop thrombosis.…”

Section: Introductionmentioning

confidence: 99%

Reduced Alpha-2-Antiplasmin Levels in the Nephrotic Syndrome

Rb¹,

Rm²,

Levitan³

et al. 1985

Nephron

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Venous and arterial thromboembolism frequently complicate the nephrotic syndrome. Increased platelet aggregation, high levels of fibrinogen and other procoagulants, and depressed levels of antithrombin III and plasminogen are commonly cited as reasons. Less attention has been paid to changes in the hemostatic system which might protect against thrombosis. We found a high frequency of reduced α₂-antiplasmin levels in 40 patients with nephrotic syndrome, correlating with serum albumin and with antithrombin III levels. Since α₂-antiplasmin is a major determinant of the sensitivity of fibrin thrombi to lysis, and since reduced levels would be expected to promote fibrinolysis, we conclude that in many patients with nephrotic syndrome depressed antiplasmin levels may help reduce the risk of thrombosis posed by diminished antithrombin III levels.

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Platelet hyperaggregability as a consequence of the nephrotic syndrome

Cited by 26 publications

References 14 publications

Platelet abnormalities in nephrotic syndrome

Platelet abnormalities in nephrotic syndrome

Haemostatic measurements in childhood nephrotic syndrome

Reduced Alpha-2-Antiplasmin Levels in the Nephrotic Syndrome

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