A 55-year-old male, ex-smoker and with poorly controlled arterial hypertension, who started hemodialysis at 40 years of age (2000) through a left radiocefable kidney transplant due to a malignant nephroangiopathy in 2001.
As other antecedents, he had a popliteal aneurysm in the right lower limb, which was operated by femoropopliteal bypass of the saphenous vein due to thrombosis that required acute supracondylar amputation.
In 2007, AVF was closed due to venous aneurysm degeneration.
In 2015, a true asymptomatic AHA of 4.5 cm in diameter was diagnosed by Doppler ultrasound, confirmed by contrast-enhanced computed tomography (CT-angiography).
Aneurysmal resection and interposition of ipsilateral basilic vein were performed.
At 6 months follow-up, bypass remains permeable and without complications.
HAAs have been described in the context of AVF for hemodialysis, although most of these are anastomotic or venous pseudoaneurysms.
True degenerative aneurysms are very rare, with an estimated incidence of 0.17%1.
True AHAs are more frequently related to radiocephalic AVF (60%), followed by brachyocephalic ones and usually appear 7-19 years after its creation3.
Unlike aortic, femoral and popliteal aneurysms, AHAs do not seem to be associated with synchronous aneurysms in other locations2.
All this suggests an etiopathogenic origin different from the rest of true degenerative aneurysms.
Several mechanisms have been described that cause a significant increase in the arterial diameter after the creation of an AVF; on the one hand, the increase in intra-arterial blood flow generates fissures in the elastic fibers in the internal lamina causing endothelial growth.
These mechanisms are not prevented or avoided by closure or thrombosis of AVF3.
Renal transplantation has been associated with arterial aneurysmal progression proximal to AVF and steroid treatment has also been associated with an increased incidence of AAH4,6,7.
The two cases presented here were renal patients who received treatment for more than 10 years and developed HAA at 15 and 25 years after the creation of the AVF, respectively.
Its most common clinical manifestation is asymptomatic pulsatile mass, although it can cause pain and paresthesia due to local compression.
Distal embolization has been observed in 28-30% of cases, the rest of ischemic presentations are unusual and rupture is extremely rare 3,8,9.
The initial diagnostic test is color Doppler ultrasonography, although CT angiography is the most commonly used technique for surgical planning10.
Due to its low frequency, therapeutic indications are usually based on those accepted for popliteal aneurysms.
In general, surgical treatment is indicated in asymptomatic HAA from 3 cm. In those between 2-3 cm surgery is recommended when they present compressive symptoms or distal embolization8.
The first-line treatment is usually aneurysm resection, maintaining arterial continuity by direct suture if possible.
If revascularization is required, autologous grafts should be preferred; if they are not available, prostatic or allografts should be used3.8-10.
In a systematic review published in 2015 with 12 eligible articles and 23 cases described in total, the mean patency was 12 months (1-38 months) after self-injection interposition and 610 months (1-48 months).
Although systematic ultrasound follow-up in patients with an AVF is not recommended, probably because it is not cost-effective, it would be reasonable to perform a physical examination of the AVF in the follow-up appointments or in the sessions.
If aneurysmal degeneration of AVF is suspected, it would be advisable to request a standardized ultrasound control in order to identify it early and avoid possible thromboembolic and/or compressive complications.
