首页> 外文期刊>American Journal of Kidney Diseases: The official journal of the National Kidney Foundation >Medial fibrosis, vascular calcification, intimal hyperplasia, and arteriovenous fistula maturation.
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Medial fibrosis, vascular calcification, intimal hyperplasia, and arteriovenous fistula maturation.

机译:内侧纤维化,血管钙化,内膜增生和动静脉瘘成熟。

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BACKGROUND: Arteriovenous fistulas (AVFs) for hemodialysis frequently fail to mature because of inadequate dilation or early stenosis. The pathogenesis of AVF nonmaturation may be related to pre-existing vascular pathologic states: medial fibrosis or microcalcification may limit arterial dilation, and intimal hyperplasia may cause stenosis. STUDY DESIGN: Observational study. SETTING & PARTICIPANTS: Patients with chronic kidney disease (N = 50) undergoing AVF placement. PREDICTORS: Medial fibrosis, microcalcification, and intimal hyperplasia in arteries and veins obtained during AVF creation. OUTCOME & MEASUREMENTS: AVF nonmaturation. RESULTS: AVF nonmaturation occurred in 38% of patients despite attempted salvage procedures. Preoperative arterial diameter was associated with upper-arm AVF maturation (P = 0.007). Medial fibrosis was similar in patients with nonmaturing and mature AVFs (60% +/- 14% vs 66% +/- 13%; P = 0.2). AVF nonmaturation was not associated with patient age or diabetes, although both variables were associated significantly with severe medial fibrosis. Conversely, AVF nonmaturation was higher in women than men despite similar medial fibrosis in both sexes. Arterial microcalcification (assessed semiquantitatively) tended to be associated with AVF nonmaturation (1.3 +/- 0.8 vs 0.9 +/- 0.8; P = 0.08). None of the arteries or veins obtained at AVF creation had intimal hyperplasia. However, repeated venous samples obtained in 6 patients during surgical revision of an immature AVF showed venous neointimal hyperplasia. LIMITATIONS: Single-center study. CONCLUSION: Medial fibrosis and microcalcification are frequent in arteries used to create AVFs, but do not explain AVF nonmaturation. Unlike previous studies, intimal hyperplasia was not present at baseline, but developed de novo in nonmaturing AVFs.
机译:背景:用于血液透析的动静脉瘘(AVF)通常由于扩张不足或早期狭窄而无法成熟。 AVF不成熟的发病机制可能与先前存在的血管病理状态有关:内侧纤维化或微钙化可能会限制动脉扩张,而内膜增生可能导致狭窄。研究设计:观察性研究。地点和参与者:患有慢性肾脏疾病(N = 50)的患者正在接受AVF放置。预测者:在创建AVF时获得的动脉和静脉内纤维化,微钙化和内膜增生。结果与测量:AVF未成熟。结果:尽管尝试了挽救程序,但仍有38%的患者发生了AVF不成熟。术前动脉直径与上臂AVF成熟相关(P = 0.007)。非成熟和成熟AVF患者的内侧纤维化相似(60%+/- 14%vs 66%+/- 13%; P = 0.2)。 AVF未成熟与患者年龄或糖尿病无关,尽管这两个变量均与严重的内侧纤维化显着相关。相反,尽管男性和女性的内侧纤维化相似,但女性的AVF未成熟度高于男性。动脉微钙化(半定量评估)往往与AVF不成熟有关(1.3 +/- 0.8对0.9 +/- 0.8; P = 0.08)。 AVF创建时获得的动脉或静脉均无内膜增生。然而,在不成熟的AVF的外科翻修过程中,有6例患者获得了重复的静脉样本,显示出静脉内膜增生。局限性:单中心研究。结论:内侧纤维化和微钙化在创建AVF的动脉中很常见,但不能解释AVF未成熟。与以前的研究不同,内膜增生并不存在于基线,而是在未成熟的AVF中从头发展。

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