Platelet thromboxane formation and BTG levels after intensive charcoal HP in uremics or regular hemodialytic treatment (RHT).
Vascular tissues from uremic patients show increased prostaglandin synthesizing capacity while uremic platelets have decreased thromboxane synthesis. It has been suggested that the platelet defects in uremia are partially corrected by hemodialysis and a correlation with the levels of guanidinsuccinic acid, phenolic acid, creatinine or urea has been demonstrated. In our study 6 patients with end-stage renal disease on RHT, underwent, daily and for ten days, two-hours hemoperfusion, in order to obtain lower levels of toxic metabolites such as creatinine (less than 6 mg/dl.). Before and after this intensive treatment we have evaluated BTG plasmatic levels and thromboxane formation by platelets after thrombin and arachidonic acid stimulation. The thromboxane formation was not increased following this treatment, whereas BTG plasmatic levels were significantly diminished.
D000328:Adult; D001609:Beta-Globulins / Q000097:blood*; D001792:Blood Platelets / Q000378:metabolism*; D002606:Charcoal; D006464:Hemoperfusion; D006801:Humans; D007676:Kidney Failure, Chronic / Q000097:blood*; D008875:Middle Aged; D006435:Renal Dialysis; D013929:Thromboxane B2 / Q000096:biosynthesis; D013931:Thromboxanes / Q000096:biosynthesis*; D014511:Uremia / Q000097:blood*; D001620:beta-Thromboglobulin / Q000097:blood*
D001609:Beta-Globulins; D013931:Thromboxanes; D001620:beta-Thromboglobulin; D002606:Charcoal; D013929:Thromboxane B2