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AGRENAM

The set of reagents for studying platelet aggregation activity (AGRENAM) according to TU 9398-277-05595541-2008 is intended for investigating platelet aggregation in human plasma using the method of optical aggregatometry. The goal is to identify the activation or impairment of the functions of these cells for the diagnosis of acquired and inherited platelet disorders.

The AGRENAM kit, consisting of inducers of adenosine 5'-diphosphate (ADP), collagen, and ristocetin, is designed for the investigation of platelet aggregation activity.

Adenosine 5'-diphosphate (ADP) is used as an inducer in routine platelet aggregation analysis to determine their dysfunction or activation. ADP is localized in the dense granules of platelets, and by using ADP, platelets activate themselves, thereby contributing to changes in shape, degranulation, and aggregation.

Collagen is used for investigating platelet aggregation to diagnose Glanzmann's thrombasthenia, Wiskott-Aldrich syndrome, collagen receptor defects (GpVI and GpIa/IIa), and storage pool deficiencies.

Ristocetin is used for investigating platelet aggregation to diagnose von Willebrand disease.

Method principle: In vivo, platelets participate in primary hemostasis by first adhering and then aggregating at the site of vascular injury. In vitro platelet aggregation can be initiated by adding various inducers: ADP, collagen, ristocetin, thrombin, adrenaline, arachidonic acid, allowing for the differential diagnosis of platelet disorders. Inducers added to platelet-enriched plasma induce platelet adhesion. In this process, normal platelets change their shape, release endogenous ADP, and aggregate. Platelet aggregation studies are conducted in an optical or impedance aggregometer. Optical devices record changes in light transmission through a cuvette with platelet-enriched plasma during platelet aggregation induced by an aggregating agent, while impedance devices register aggregation in whole blood by changes in electrical conductivity.

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Set composition:

  • Adenosine 5'-diphosphate (ADP), lyophilized (1 ml/vial) with a concentration of 0.2 mM/l – 2 vials;
  • Collagen, lyophilized (1 ml/vial) with a concentration of 0.2% – 2 vials;
  • Ristocetin, lyophilized (0.5 ml/vial) with a concentration of 1.5% – 2 vials.

Each vial with lyophilized aggregation inducers is intended for conducting from 10 to 20 analyses depending on the analyzer used and the concentration.

Results interpretation: In the normal plasma of healthy individuals, the level of platelet aggregation activity under the action of ADP is 50-80%; Aggregation under the action of ADP is absent in Glanzmann's thrombasthenia, reduced in Wiskott-Aldrich syndrome, and the second wave of aggregation is absent in storage pool deficiency. Aspirin at a dose of 0.25 g/day completely blocks the aggregation-release reaction (the second wave of aggregation is absent).

In the normal plasma of healthy individuals, the level of platelet aggregation activity under the action of collagen is 50-80%; Platelet aggregation under the action of collagen is sharply reduced or completely absent in Glanzmann's thrombasthenia, Wiskott-Aldrich syndrome, collagen receptor defects, storage pool deficiency, and disorders of arachidonic acid metabolism.

In the normal plasma of healthy individuals, the level of platelet aggregation activity under the action of ristocetin is 55-90%; Aggregation under the action of ristocetin is absent or reduced in Bernard-Soulier syndrome or von Willebrand disease types I or III. Aggregation 1.5-2 times higher than normal may be observed in platelet-type von Willebrand syndrome.