BACKGROUND AND OBJECTIVE: Patients with end-stage renal disease or advanced cirrhosis develop bleeding disorders characterized by defective interaction of platelets with damaged subendothelium. The anemia associated with both clinical entities has a negative influence on hemostasis. We evaluated alterations of platelet function in patients suffering from end-stage renal disease (n=21) or hepatic cirrhosis (n=20) using standard aggregometric techniques and the recently developed platelet function analyzer (PFA-100 ). The impact of low hematocrit was also analyzed. DESIGN AND METHODS: The hemostatic capacity of platelets was tested in the PFA-100 using citrated blood and standard cartridges containing collagen-ADP (COL-ADP) or collagen-epinephrine (COL-Epi). The hemodynamic influence of hematocrit was also evaluated in blood aliquots in which hematocrit was experimentally increased by adding red blood cells from the same patient. RESULTS: Aggregation studies demonstrated abnormal responses to several agonists in both group of patients. Closure times obtained by the PFA-100 for control blood samples were 87+/-3 sec for COL-ADP and 113+/-5 sec with COL-EPi cartridges. Closure times in uremic and cirrhotic patients with average hematocrits of 0.26 and 0.27 respectively were significantly prolonged (139+/-12 and 125+/-14 sec, respectively with COL-ADP and 194+/-29 and 151+/-15 sec with COL-Epi cartridges). A 5% increase in the hematocrit caused a reduction in the closure time to 111+/-7 sec (COL-ADP) and 143+/-14 sec (COL-Epi) in the uremic group and to 86+/-4 sec (COL-ADP) and 115+/-16 sec (COL-Epi) in the cirrhotic group. Our studies confirm the platelet dysfunction in uremic and cirrhotic patients. INTERPRETATION AND CONCLUSIONS: The PFA-100 device proved to be useful for testing alterations of primary hemostasis in these acquired disorders and was sensitive enough to detect modifications in hemostasis caused by elevations in hematocrit. Conventional aggregometric tests were able to identify the intrinsic platelet abnormality in uremic and cirrhotic conditions, while the PFA-100 seemed more sensitive in detecting the negative influence of the hematocrit reduction.
BACKGROUND AND OBJECTIVE:Patients with end-stage renal disease or advanced cirrhosis develop bleeding disorders characterized by defective interaction of platelets with damaged subendothelium. The anemia associated with both clinical entities has a negative influence on hemostasis. We evaluated alterations of platelet function in patients suffering from end-stage renal disease (n=21) or hepatic cirrhosis (n=20) using standard aggregometric techniques and the recently developed platelet function analyzer (PFA-100 ). The impact of low hematocrit was also analyzed. DESIGN AND METHODS: The hemostatic capacity of platelets was tested in the PFA-100 using citrated blood and standard cartridges containing collagen-ADP (COL-ADP) or collagen-epinephrine (COL-Epi). The hemodynamic influence of hematocrit was also evaluated in blood aliquots in which hematocrit was experimentally increased by adding red blood cells from the same patient. RESULTS: Aggregation studies demonstrated abnormal responses to several agonists in both group of patients. Closure times obtained by the PFA-100 for control blood samples were 87+/-3 sec for COL-ADP and 113+/-5 sec with COL-EPi cartridges. Closure times in uremic and cirrhoticpatients with average hematocrits of 0.26 and 0.27 respectively were significantly prolonged (139+/-12 and 125+/-14 sec, respectively with COL-ADP and 194+/-29 and 151+/-15 sec with COL-Epi cartridges). A 5% increase in the hematocrit caused a reduction in the closure time to 111+/-7 sec (COL-ADP) and 143+/-14 sec (COL-Epi) in the uremic group and to 86+/-4 sec (COL-ADP) and 115+/-16 sec (COL-Epi) in the cirrhotic group. Our studies confirm the platelet dysfunction in uremic and cirrhoticpatients. INTERPRETATION AND CONCLUSIONS: The PFA-100 device proved to be useful for testing alterations of primary hemostasis in these acquired disorders and was sensitive enough to detect modifications in hemostasis caused by elevations in hematocrit. Conventional aggregometric tests were able to identify the intrinsic platelet abnormality in uremic and cirrhotic conditions, while the PFA-100 seemed more sensitive in detecting the negative influence of the hematocrit reduction.