Uremic patients may have thrombocytopenia, average of about 100 x 109/l, bleeding and clotting time is normal, capillary fragility may increase. The pathogenesis includes the following three aspects:
Platelet dysfunction: accumulation of some toxic substances in the blood of patients with uremia, the content and activity of platelet factor III decreased release of obstacles, reducing effectiveness, prothrombin consumption and thromboplastin generation poor, platelet adhesion and aggregation decreased.
Fibrinolytic activity decreased: uremia, as urokinase inhibitors significantly increased or decreased significantly due to plasminogen activation factor, so the fibrinolytic activity decreased, fibrinogen caused by organs of fibrin deposition. Localized fibrin in the kidney is degraded and produces a large number of fibrin degradation products. Large molecular fragments of fibrin degradation products with antithrombin strongly, inhibit platelet function, the formation of the small molecular interference thromboplastin; fibrin degradation product fragments could inhibit fibrin monomer polymerization, obstructing blood clot. Therefore, the appearance of fibrin degradation products aggravates the tendency of uremia hemorrhage.
The change of blood coagulation factors: Uremia can slightly prolonged prothrombin time prolonged, this may be due to uremic toxic substances inhibit factorⅱ、ⅴ、ⅶ、ⅹ, he vitality. At the same time, long-term use of antibiotics causes intestinal sterilization syndrome, which can cause the absorption and synthesis of vitamin K. These factors are also part of the cause of the bleeding tendency.