We investigated shear‐induced platelet aggregation (SIPA) in 30 patients with chronic renal failure (CRF) undergoing haemodialysis. 26 patients showed a significant decrease in SIPA at high shear stress but no change in SIPA at low shear stress. The former reaction reflects the interaction between plasma von Willebrand factor (vWF) and its platelet receptors, glycoprotein (GP) Ib‐IX and lIb/ IlIa complex, whereas the latter is assumed to involve the binding of plasma fibrinogen to GP IIb/IIIa complex. These SIPA profiles in CRF patients after haemodialysis showed almost no change compared to those before haemodialysis.
The ratio of ristocetin cofactor/vWF antigen in plasma was slightly lower in CRF patients than in controls (P<0.01). However, the level of GPIb antigen in the platelets of these patients was significantly reduced (42.1±20‐3% of normal platelets), with partial destruction of GPIb antigen. The number of vWF receptors on the GPIb molecule was quantitated using the GPIb‐binding protein alboaggregin‐B (AL‐B), purified from the snake venom of Trimeresurus albolabris. AL‐B bound to GPIb at a total of 48 760±9944 molecules per normal platelet and a Kd of 85.44±15.70 nM at saturation. In contrast, binding in CRF platelets was 22 980±6395 molecules per platelet and Kd was 50.08±13.83 nM. Taking these results together, we conclude that the impaired SIPA found in CRF patients is due to both abnormalities in plasma vWF and in its platelet GPIb receptor.
We report the case of a 57-year-old female suffering from recurrent malignant undifferentiated pleomorphic sarcoma of the left atrium. Metastasis to the posterior mediastinum was detected upon first presentation. Incomplete resections were carried out twice before mitral valve replacement was finally performed. The tumor recurred 16 months later and was treated with radiation therapy, which has proved to be effective in bringing about tumor regression for 2 years, to date. The patient has survived for 7 years since the first surgery.
In this study, we report a case of a patient on dialysis who presented necrotic lesions on the legs and penile ulceration 7 years after a mechanical aortic valve replacement. The diagnosis of calciphylaxis was not confirmed even after skin biopsy, and multidisciplinary management was not initiated until the patient was admitted with septic shock. Cardiovascular surgeons should be aware of warfarin-induced calciphylaxis, whose pathophysiology differs from that of atherosclerosis. Considering poor long-term survival of dialysis patients, mechanical valves should be reserved only for those patients whose estimated survival is longer than the time taken for a biological valve to deteriorate.
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