Decreased platelet factor 3 activity, abnormal platelet adhesiveness, and abnormal platelet aggregation all contribute to platelet abnormalities
The simplest acute treatment for the bleeding patient with uremic platelet dysfunction is desmopressin (dDAVP), which is effective in at least 50% of such patients by increasing Factor VIII:von Willebrand Factor multimers from endothelial storage (platelets bind to collagen on vascular endothelium via vWF through the GP1B receptor, thus increases in vWF can enhance adhesiveness). This can be administered intravenously over 15-30 minutes or intranasally and demonstrates improvement within one hour and lasts 4 to 24 hours. Tachyphylaxis develops following the second dose, likely due to depletion of multimers from endothelial storage
Effective treatment in severe acute bleeding often involves transfusion of desmopressin, cryoprecipitate and packed red blood cells. Each independently has its own mechanism addressing platelet dysfunction, together producing an additive effect. Additional therapies include conjugated estrogens and erythropoietin
Platelet transfusion should only be used in combination with desmopressin, cryoprecipitate and PRBCs, for soon after entering a uremic environment, platelets become dysfunctional.
Renal Failure and Platelet Dysfunction
- Mechanism: decreased platelet factor 3 activity, abnormal platelet adhesiveness, abnormal platelet aggregation
- Treatment: desmopressin first line. Consider cryoprecipitate, PRBCs, conjugated estrogen, EPO