guanidinosuccinic acid/hemorrhage

Platelet aggregation induced by ADP can be inhibited by plasma from uremic patients or by toxins isolated from their plasma, e.g. guanidinosuccinic acid, methylguanidine, phenol and hydroxyphenylacetic acids. Since these chemical substances can interfere with energy metabolism in tissues other than

The effect of various small and middle molecular substances on blood platelet glycolysis was studied in vitro. Creatinine inhibited glucose utilization only at a concentration of 30 mg/dl; no effect of urea was found. o-Hydroxyphenolic acid and guanidinosuccinic acid, which were supposed to

Globin synthesis was measured by incubating washed packed red cells with a balanced amino acid mixture and 14C-Histidine. After globin had been isolated from the haemolysate the 14C-incorporation rate per 10 mg globin per min was estimated. With regard to globin synthesis no differences existed

Numerous hemostatic abnormalities have been associated with acute and chronic renal disease. The most common abnormalities are defective platelet aggregation, decreased platelet adhesiveness, decreased platelet factor-3 availability, and prolongation of the bleeding time. Among the above platelet

Guanidinosuccinic acid is an aberrant metabolite isolated 40 years ago in the blood and urine of uremic subjects and a suspect in the toxicity associated with renal failure. It plays a minor role in the bleeding diathesis of uremia, contributes to the methyl group deficiency of dialysis patients,