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The etiology of pseudoaneurysms in this location is multifactorial, however, an association with chronic rejection must be considered. Though rare, the development of pseudoaneurysms at the donor renal-external iliac artery anastomosis results in high rates of transplant nephrectomy. Less invasive endovascular techniques offer a new therapeutic option in this challenging scenario notwithstanding the fact that they require further validation.

Surgical excision of anastomotic pseudoaneurysms results in high rates of allograft loss. Less invasive techniques have a place in selected cases.

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Objective-Many gene products involved in oxidation and inflammation are implicated in the pathogenesis of atherosclerosis. We investigated paraoxonase 2 (PON2), 5-lipoxygenase (5-LO), and 5-LO activating protein (FLAP) expression and malondialdehyde (MDA) levels in carotid lesions to assess their involvement in plaque formation. Methods and Results-We measured gene expression and MDA levels in atherosclerotic plaques from 59 patients undergoing carotid endarterectomy, and in plaque-adjacent tissue from 41/59 patients. Twenty-three fetal carotids and 6 mammary arteries were also investigated. Real-time polymerase chain reaction and immunohistochemistry revealed decreased PON2 expression in plaques versus adjacent regions (PϽ0.005, PϽ0.001, respectively), mammary arteries (PϽ0.031, PϽ0.001, respectively), and fetal carotids (both PϽ0.001). mRNA levels of 5-LO and FLAP were higher (PϽ0.038, PϽ0.005, respectively) in lesions versus fetal carotids. MDA was higher in plaques versus plaque-adjacent tissue and fetal carotids. PON2 mRNA was downregulated by oxidative stress in 5 ex vivo experiments, thereby indicating its possible atheroprotection role. Conclusions-We demonstrate that PON2 mRNA and protein are decreased in plaques versus plaque-adjacent tissue, mammary arteries, and fetal carotids. Our data indicate that the protective effect of PON2 could fail during atherosclerosis exacerbation; this was confirmed by the increase of MDA levels. Key Words: atherosclerosis Ⅲ paraoxonase 2 (PON2) Ⅲ carotid plaque Ⅲ oxidative stress Ⅲ fetal carotid and mammary artery C arotid atherosclerotic plaques are important risk factors for stroke, which is in turn a major cause of morbidity and mortality. 1 Lipid oxidation plays a key role in the pathogenesis of atherosclerosis. 2,3 The production of oxidized molecules is related to an imbalance between oxidant and antioxidant factors. 3,4 Accumulation of oxidized low-density lipoprotein (ox-LDL) in artery walls is an initiating event of fatty streak development. 5,6 Moreover, oxidized products give rise to inflammatory events which, in turn, lead to the progression of plaques. 7,8 Increasing evidence suggests that genes such as paraoxonases (PONs) and lipoxygenases (LOs), which are involved in oxidative stress and inflammation, play key roles in the onset and progression of atherosclerotic plaques. 9,10 The PON family consists of 3 genes (PON1, PON2, and PON3) that have similar antioxidant properties but different expression profiles: PON1 and PON3 are expressed in the liver and circulate in close association with apolipoprotein A-1 in high-density lipoprotein (HDL), 11,12 whereas PON2 is expressed in many different types of tissues and cells including cells of the artery wall. 13 PON polymorphisms are associated with atherosclerosis, diabetes, prostate cancer, Alzheimer dementia, Parkinson disease, and acquired hearing loss. 14 -20 Interestingly, a study of PON2-deficient mice showed that PON2 protected against atherogenesis in vivo by modulating lipoprotein properties, thereby ...