Platelet abnormalities in nephrotic syndrome

Abstract

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.

Predictive value of platelet indices in children with idiopathic nephrotic syndrome

“…In 1981, Walter et al reported increased platelet counts and spontaneous aggregation in children with nephrotic syndrome, which normalized after long-term remission (2). The exact mechanism of increased platelet counts has not been completely understood in nephrotic syndrome.…”

“…The exact mechanism of increased platelet counts has not been completely understood in nephrotic syndrome. However, a correlation has been reported between hypoalbuminemia and hypercholesterolemia with platelet hyper-aggregation and elevated platelet counts (2)(3)(4).…”

“…Platelets play an essential role in primary hemostasis. They are important mediators of immunomodulation and inflammatory reactions by releasing different cytokines and growth factors (1,2).…”

Study of A Disintegrin and Metalloproteinase with ThromboSpondin Type 1 Repeats 13 (ADAMTS 13) in Children with Idiopathic Nephrotic Syndrome

“…Platelet hyperaggregability, increased release of active substances, and elevated surface expression of activation-dependent platelet markers have been documented. The mechanisms underlying platelet alterations are probably due to changes in plasma levels of platelet-interfering proteins and lipid changes, as a consequence of nephrosis [16].…”

Correlation of serum level of albumin with platelet count and platelet aggregation assessed by adenosine diphosphate agonist in children with nephrotic syndrome

“…Platelet are considered as an important agent of thrombosis among NS patients. 6 The gold standard for platelet aggregation requires the use of adenosine diphosphate (ADP) agonists, which are dense granule degranulation products that directly induce platelet aggregation, unlike thrombin and collagen which only trigger ADP and TXA2 release. 7 However, this examination may be affected by various medications such as NSAIDs, platelet receptor antagonists (Abciximab, Clopidogrel), glycoprotein IIb/IIIa inhibitor (Eptifibatide), phosphodiesterase inhibitor (Dipiridamol), anticoagulants (heparin, warfarin), diuretics, and vasodilators.…”