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HEMATOLOGY: ISSUES IN THE DIALYSIS PATIENT: Platelet Dysfunction and End‐Stage Renal Disease
Author(s) -
Kaw Dinkar,
Malhotra Deepak
Publication year - 2006
Publication title -
seminars in dialysis
Language(s) - English
Resource type - Journals
SCImago Journal Rank - 0.899
H-Index - 78
eISSN - 1525-139X
pISSN - 0894-0959
DOI - 10.1111/j.1525-139x.2006.00179.x
Subject(s) - medicine , hemodialysis , dialysis , hemostasis , platelet , peritoneal dialysis , hypervolemia , hematocrit , platelet activation , thrombosis , end stage renal disease , kidney disease , cardiology , blood volume
Patients with end‐stage renal disease (ESRD) develop hemostatic disorders mainly in the form of bleeding diatheses. Hemorrhage can occur at cutaneous, mucosal, or serosal sites. Retroperitoneal or intracranial hemorrhages also occur. Platelet dysfunction is the main factor responsible for hemorrhagic tendencies in advanced kidney disease. Anemia, dialysis, the accumulation of medications due to poor clearance, and anticoagulation used during dialysis have some role in causing impaired hemostasis in ESRD patients. Platelet dysfunction occurs both as a result of intrinsic platelet abnormalities and impaired platelet–vessel wall interaction. The normal platelet response to vessel wall injury with platelet activation, recruitment, adhesion, and aggregation is defective in advanced renal failure. Dialysis may partially correct these defects, but cannot totally eliminate them. The hemodialysis process itself may in fact contribute to bleeding. Hemodialysis is also associated with thrombosis as a result of chronic platelet activation due to contact with artificial surfaces during dialysis. Desmopressin acetate and conjugated estrogen are treatment modalities that can be used for uremic bleeding. Achieving a hematocrit of 30% improves bleeding time in ESRD patients.