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

Pao Hsien Chu*, Shih Ming Jung, Chi Hsiao Yeh, Hsueh Hua Wu, Tzu Fang Shiu, Hung Chung She, Ngan Ming Tseng

*Corresponding author for this work

Research output: Contribution to journalJournal Article peer-review

4 Scopus citations


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±2.14×109/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.

Original languageEnglish
Pages (from-to)995-999
Number of pages5
Issue number11
StatePublished - 11 2008


  • Apoptosis
  • Fistula
  • Thrombus


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