الفهرس 
HEMOSTASISOnly 14 pages are availabe for public view
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Abstract
In ESRD patients, a tendency to bleed is a common problem and is an important cause of both morbidity and mortality. The clinical manifestations of bleeding tendency have been well described and vary from ecchymoses, epistaxis, bleeding from gums and venipuncture sites to overt gastrointestinal bleeding.
The potential for bleeding in patients with uremia is a significant clinical concern especially when surgical or other invasive procedures are required. This bleeding tendency is mainly due to abnormalities in primary hemostasis, in particular, platelet dysfunction.
It is thought that uremic blood alters platelet function to result in abnormal platelet aggregation, secretion and adhesion to the vascular endothelium. The pathogenesis of altered platelet function is considered multifactorial and is not yet fully understood. Anemia through its rheological effect further compounds the bleeding disorder.
Platelet dysfunction in uremic patients is partially due to uremic toxins present in circulating blood. Some substances that inhibit platelet function in concentrations attained in uremic plasma include urea, guanidine – succinate, parathyroid hormone, phenol and tryptophan products.
These substances accumulate in patients with RF due to reduced clearance. This may explain the improvement in hemostasis seen after effective dialysis. Although dialysis improves platelet abnormalities and reduces, but does not eliminate the risk of hemorrhage.
The platelet function analyzer-100 is a global test that evaluates the ability of platelets activated in a high shear enviroment to occlude an aperture in a membrane treated with CEPI or CADP.
In this study we evaluated the hemostatic function among ESRD patients before and after hemodialysis session by PFA-100 analyzer. The CT detected by the PFA-100 was significantly longer among all patients before hemodialysis session compared to controls. CT was significantly shorter among all patients after hemodialysis session compared to all patients before hemodialysis session, but it was still significantly longer among all patients after hemodialysis session compared to controls.
We found a highly significant difference between patient and control group and also between patients before and after hemodialysis session regarding Hb and Hct values. Also we found no significant difference between the three patients’ subgroups (HN, DN and patients with other causes of RF) before and after hemodialysis session regarding clinical and laboratory data, while there was a highly significant difference between HN patients and patients with other causes of RF and between DN patients and patients with other causes of RF regarding age.
There was no significant difference between male and female patients regarding CT neither before nor after hemodialysis session. There was no correlation between CT and clinical data (age, duration of illness and heparin dose) and also laboratory data (Hb, Hct & platelet count) neither before nor after hemodialysis session.
In conclusion, as regards the results of PFA-100 our study confirmed that there was platelet dysfunction in ESRD patients, and hemodialysis had the ability to correct some part of these hemostatic disturbances. The PFA-100 system may become a useful tool for evaluation of primary hemostasis in patients with ESRD, as it is a sensitive, specific, reproducible, easy to perform and non invasive test for platelet-related primary hemostasis.