Expression of caspase‐3‐dependent apoptosis in mural thrombi leukocytes

Abstract

Failure of arteriovenous access is mostly due to graft thrombosis and multifactorial, with medical and surgical etiologies. Apoptosis of blood cells, such as macrophages, lymphocytes and eosinophils, may play an important role in thrombus formation. We also investigated caspase-3-dependent apoptosis in thrombi. We recorded clinical parameters in 43 consecutive patients with vascular access failure (13 men, 30 women; mean age+/-SD, 64.6+/-14.2 years) who underwent surgical thrombectomy. Major presentations included absent (92%) and/or near near-absent (16%) flow through the access during hemodialysis. Cardiovascular risk factors were hypertension (70%), hyperlipidemia (47%), diabetes mellitus (47%), chronic obstructive pulmonary disease (12%), heart failure (12%), coronary artery disease (21%), and stroke (16%). Laboratory data included hemoglobin level of 100+/-17 g/L, total white blood cell count of 7.65+/-2.14 x 10(9)/L, and platelet count of 205.6+/-57.9 1000/ìL. Abnormal biochemistry data included elevated blood urea nitrogen level of 63.5+/-24.4 mg/dL and creatinine level of 8.6+/-4.0 mg/dL (normal <1.4 mg/dL). Thrombi were characterized by apoptosis (32%) in a caspase-dependent pathway in all types of leukocytes. Thrombi in arteriovenous access failure demonstrate apoptosis by means of the caspase-3 pathway in white blood cells.