1988
DOI: 10.1177/039139888801100206
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Mechanisms of Platelet Aggregation Disturbances and Their Relation to Treatment in Patients with Chronic Uremia

Abstract: We have examined platelet aggregation in patients with chronic uremia using ADP, thrombin and calcium ionophore A23187 as inducers. The study was performed on patients treated conservatively, by hemodialysis and peritoneal dialysis. Platelet aggregation was most significantly depressed in patients treated conservatively and by hemodialysis. Different mechanisms are responsible for platelet dysfunction.

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Cited by 7 publications
(4 citation statements)
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“…Activated platelets release ADP, serotonin, and other factors that maintain their stimulation. As a consequence, platelets are becoming 'exhausted' and ex hibit in in vitro experiments signs of acquired storage pool disease [6][7][8],…”
Section: Discussionmentioning
confidence: 99%
“…Activated platelets release ADP, serotonin, and other factors that maintain their stimulation. As a consequence, platelets are becoming 'exhausted' and ex hibit in in vitro experiments signs of acquired storage pool disease [6][7][8],…”
Section: Discussionmentioning
confidence: 99%
“…As could be shown, for example, after ingestion of ASA, as well as in the case of patients with myeloproliferative syndromes, uremia and known hereditary platelet deficiencies, hypoaggregability can be reliably detected. Hypoaggregability is a well-known occurrence in myeloproliferative syndromes [6,9], ure mia [10][11][12] and other illnesses, but not enough is known about its progress and sus ceptibility.…”
Section: Discussionmentioning
confidence: 99%
“…Reduced quantity of such platelets in hemodialyzed patients is probably one of the factors responsible for the depressed platelet aggregation induced by ADP and other agonist [2,4]. …”
Section: Discussionmentioning
confidence: 99%