Anatomic Characteristics and Natural History of Renal Artery Aneurysms During Longitudinal Imaging Surveillance

Abstract

There were a total of 312 CAS procedures (n ¼ 299 patients) and 344 CEA procedures (n ¼ 335) in this time period. For patients who had reoperation on the same carotid vessel (n ¼ 5 for CAS, n ¼ 5 for CEA), we used the last documented ultrasound prior to the date of reoperation. These ultrasounds were used to identify ECA occlusions and in-stent restenosis using consensus panel velocity criteria.Results: There were 210 CAS patients with follow-up ultrasounds (67%), and there were 207 CEA patients with follow-up ultrasounds in our system (60%). The average follow-up of CAS was significantly shorter than the CEA group (0.7 vs 1.7 years; P < .001), and CAS patients were more likely to take Plavix (97% vs 35%; P < .001). All other variables were similar between groups. We identified significantly more occluded ECA in the CAS ( 14) compared with the CEA (4) group (P ¼ .03). Additionally, eight (57%) of 14 arteries with ECA occlusions had >50% ISR, whereas 48 (26%) of 186 arteries without ECA occlusions had >50% ISR (P ¼ .02) (Fig).Conclusions: This is the first demonstration of increased ECA occlusion after CAS in the literature, but prior publications have identified increased external carotid stenosis. This finding was in spite of decreased follow-up time periods and increased use of Plavix in the CAS group, lending more validity to our results. A recent report identified disturbed flow in the ECA after CAS. This may be the biologic reason for these findings. The association of in-stent restenosis with ECA occlusion is also very interesting and warrants further investigation. We are currently determining whether ECA stenosis/occlusion occurs before, at the same time, or after in-stent restenosis. Establishing the timeline will be critical to identifying whether disturbed flow in the ECA has a causative role in in-stent restenosis.

Editor's Choice – Ex vivo Renal Artery Repair with Kidney Autotransplantation for Renal Artery Branch Aneurysms: Long-term Results of Sixty-seven Procedures

“…Therefore, mean rate of aneurysm growth appears highly variable and seems to be related to the initial diameter. In the authors' experience, rapid growth is rare for small aneurysms and this observation is consistent with the data from the studies of Klausner et al and Wayne et al 24,25 For these lesions, imaging follow up can be less frequent. Conversely, surgery is indicated in cases of rapid diameter growth.…”

“…Klausner et al and Wayne et al have studied the evolution of renal artery aneurysms and reported particularly slow growth, <1 mm per year. 24,25 In the present study, mean diameter growth was higher, rising to 9.2 mm in 36 months with a median growth of 3.1 mm per year. The difference between the present series and the two other publications may be explained by different patient profiles.…”

Renal artery aneurysms

“…2 Most ruptures are diagnosed at the time of presentation, and several authors have supported no rupture during the surveillance of nonoperative RAAs. 1,2,4,5,[7][8][9][10][11] Contemporary series estimate a median annualized growth rate of 0.06 to 0.6 mm. [9][10][11] The most recent and largest multiinstitutional series of nonoperative RAA surveillance found no difference in growth rate based on aneurysm morphology or calcification.…”

“…1,2,4,5,[7][8][9][10][11] Contemporary series estimate a median annualized growth rate of 0.06 to 0.6 mm. [9][10][11] The most recent and largest multiinstitutional series of nonoperative RAA surveillance found no difference in growth rate based on aneurysm morphology or calcification. 10 These same authors also report the successful surveillance of 88 aneurysms measuring 2 to 3 cm and seven aneurysms measuring >3 cm without complication or rupture during a mean of 49 months.…”

“…Approximately 70% of patients with RAA have HTN, with up to 100% affected in some series. 1,2,7,9,[11][12][13]16,17 Hypotheses for the mechanism of HTN include (1) coexistent renal artery occlusive disease, (2) distal parenchymal embolization, (3) compression or kinking of associated renal artery branches, and (4) hemodynamic changes from turbulent blood flow within the aneurysm resulting in decreased distal renal artery perfusion. 2,16 Most series suggest improvement or cure in the majority of hypertensive patients undergoing RAA reconstruction (Table II).…”