Renal Artery Aneurysm

Updated: Sep 21, 2021
Author: Lindsay Gates, MD; Chief Editor: Vincent Lopez Rowe, MD, FACS 


Practice Essentials

A renal artery aneurysm (RAA) is defined as a dilated segment of renal artery with a diameter that is more than twice the diameter of a normal renal artery.[1]  Symptomatic RAAs can cause hypertension, pain, hematuria, and renal infarction.[2]  Asymptomatic RAAs may seem benign, but the potential for rupture and fistulization increases with size. Asymptomatic patients can be referred for elective repair, but if patients are symptomatic, further investigation with possible surgical intervention should be considered.

The first published report of an RAA was in 1770 by Rouppe, who described the demise of a sailor who fell onto his right flank.[3]  Autopsy revealed a large false aneurysm with rupture. Since that time, many more case reports and case series have provided most of the data on this rare pathologic entity.[4, 5, 6, 7, 8, 9, 10, 11, 12, 13, 14, 15, 16, 17]

Because most RAAs are asymptomatic and are found incidentally during a workup for other intra-abdominal pathology, imaging studies are required only for preintervention planning or longitudinal follow-up care.

Indications for intervention in patients with a RAA include rupture, symptomatic RAA, RAA in a female who is pregnant or is contemplating pregnancy, diameter greater than 2 cm, enlarging RAA, and RAA associated with acute dissection. Currently, there is no consensus regarding the size at which an RAA should be repaired in an asymptomatic patient, though asymptomatic small (< 2 cm in diameter) RAAs usually are not considered to require treatment.


The renal arteries arise from the aorta at the level of the intervertebral disk between L1 and L2. Cadaveric studies have shown that more than one renal artery is present in 15% of cases on the right side and 20% of cases on the left.

A great deal of variety can be found in the anatomy of the renal artery and its branches, but most often the main renal artery splits into an anterior and a posterior division. Within the hilum, the anterior division gives rise to apical, anterior, and inferior segmental branches. Segmental vessels then penetrate the renal parenchyma to become lobar, interlobar, arcuate, or interlobular arteries or afferent arterioles, then finally reach the capillaries and glomeruli.[18]

Measurements of renal artery diameter can differ, depending on the imaging modality used. In one study, ultrasonography (US) reported mean renal artery measurements of 5.04 ± 0.74 mm; with angiography, they were found to be 5.68 ± 1.19 mm. In this study, the authors also determined that when accessory renal arteries were identified, the main renal artery measurements were significantly smaller in diameter than when one renal artery was present.[19]

RAAs can be classified in relation to the parenchyma of the kidney (see the image below). Extraparenchymal aneurysms predominate, comprising approximately 85% of all RAAs.[13, 17] The other 15% are intraparenchymal. Of the extraparenchymal type, roughly 70% are saccular, 20% are fusiform, and 10% are dissecting.[20]

Schematic of renal artery anatomy. The aneurysm lo Schematic of renal artery anatomy. The aneurysm location can be classified as extraparenchymal or intraparenchymal.

Of patients with RAAs, 20% present with bilateral pathology, and 30% have multiple aneurysms.[17] RAAs occur with equal frequency in men and women, though ruptures are more common in reproductive-age women.


In true aneurysms, a weakening then dilatation of all layers of the arterial wall occurs. In fibromuscular dysplasia (FMD), the degenerative fibroplasia-type changes lead to this wall weakening. Often, renal artery stenosis is associated.[21, 17] Most patients with FMD are healthy, young, hypertensive women, and on angiography the renal artery appears as a string of beads, with the aneurysm at the renal artery bifurcation.

Ehlers-Danlos syndrome is an autosomal dominant disorder characterized by fragility of medium-sized and large arteries due to type III procollagen deficiency. This condition leads to dissections and aneurysms in any artery, including the renal arteries.[22]

In false aneurysms, or pseudoaneurysms, there is a focal disruption in one or every layer of the artery that causes a saccular outpouching at the weaken area. In blunt trauma, anterior displacement of the relatively mobile kidneys with rapid deceleration generates tension in the vascular pedicle causing a fracture of the intima, predisposing it to subintimal dissection and then aneurysmal degeneration. Another mechanism involves direct arterial wall contusion against the vertebral bodies.[9]

Anastomotic leaks from previous renal artery reconstructive procedures become walled off by the body, creating a pseudoaneurysm. In this situation, the wall of the aneurysm contains only fibrotic/inflammatory tissue. Iatrogenic endovascular-related aneurysms are caused by intimal trauma and focal dissection, leading to aneurysmal degeneration. Spontaneous renal artery dissections cause aneurysms by the same mechanism described above.[23]

Intraparenchymal aneurysms are believed to arise primarily from inflammatory changes of the vessel wall. These commonly develop into microaneurysms. Intrarenal aneurysms are usually found in multiples and are often associated with arteriovenous fistulas.

Although pregnancy is not associated with an increased incidence of RAA formation, it is associated with a higher rate of rupture. The increased blood flow, intra-abdominal pressure, and vessel-wall changes due to the hormonal and metabolic changes associated with gestation are believed to be contributory. Most ruptures occur late in the pregnancy (usually in the third trimester) and are left renal artery–predominant.[6]

In the pediatric age group, RAAs are due to trauma, infection, arteritides, Kawasaki disease, or vascular dysplasias. Multiple idiopathic arterial aneurysms that include renal artery involvement have been described but are extremely rare.[24]


Many causes of RAA exist, each with different morphologies and locations along the renal artery. The lesions can be grouped into three main categories as follows.

True aneurysms include all layers of the artery and are usually inherited disorders. They can be fusiform or saccular (75% of all true RAAs) in appearance and are extraparenchymal in 90% of cases.[13, 25] Causes include the following:

  • FMD
  • Ehlers-Danlos syndrome [26]

False aneurysms (pseudoaneurysms) do not include all layers of the artery, are usually acquired, are saccular in appearance, and can be extraparenchymal or intraparenchymal. Causes include the following:

  • Blunt abdominal trauma
  • Anastomotic
  • Iatrogenic during endovascular procedures
  • Spontaneous [9]
  • Dissection
  • Mycotic [27]
  • Kawasaki disease [28]

Intrarenal aneurysms[29] are either true or false aneurysms within the renal parenchyma and account for fewer than 10% of all RAAs. They deserve special classification because their management is usually with nephrectomy or coil embolization. Causes include the following:

  • Polyarteritis nodosa
  • Tuberculosis
  • Neurofibromatosis


Autopsy studies indicate that the incidence of RAA is in the range of 0.01-0.09%.[30] In selected patients who undergo renal arteriography, a higher incidence, 0.3-1%, has been reported.[31]  In another study using computed tomography (CT) angiography (CTA), the incidence was 0.7%.[32] In one of the largest series over a 16-year period, 62 patients had RAA repair. The average age was 46 ± 18 years, and 68% were women.[33]

Overall, the average age for patients to present with RAAs is between the ages of 40 and 60 years, with a female predominance owing to the increased prevalence among patients with FMD.


The morbidity and mortality associated with elective RAA repair are very low. Many authors have reported no mortality and minimal morbidity after surgery.[8, 16, 17, 34]

The prognosis after rupture of an RAA has improved in the past few decades. One review found that mortality dropped from 62% before 1949 to 6% after 1970. Rupture of RAA during pregnancy still carries a high mortality. According to one report, renal artery rupture and its treatment resulted in death of the mother in 56% of the cases and death of the fetus in 78% of the cases.[6]

The cure rate of hypertension may be as high as 50-100% in selected patients with RAAs associated with renal artery stenosis.[5, 8, 14, 16]

Surgical repair of RAA appears to have long-term durability, though most reported series have been small and from single centers.

In a study that included 2709 patients undergoing open or endovascular elective repair of isolated RAAs between 2000 and 2011, Buck et al found no significant differences in mortality and overall complication rate between the two types of repair.[35]



History and Physical Examination


Most renal artery aneurysms (RAAs) are asymptomatic and are found incidentally during investigation of other intra-abdominal pathologies with diagnostic imaging studies such as computed tomography (CT), duplex ultrasonography (US), angiography, magnetic resonance imaging (MRI), or magnetic resonance angiography (MRA). In a small series by Dzsinich et al, only 34% (11 of 32) patients who underwent surgery were symptomatic.[8]

In asymptomatic patients, complications from RAA are relatively infrequent. In one study, 62 asymptomatic patients who had solitary saccular aneurysms with a mean size of 1.5 cm (range, 0.3-4.0 cm) were followed over a mean period of 5.7 years (median, 8 years). No ruptures, need for operations, or new symptoms developed. Eight patients (12%) did expire, but all of these deaths were unrelated to the aneurysm.[11]

In another series, 34 RAAs were managed nonoperatively and followed with serial arteriograms. Over a mean interval of 35 months, no changes were found in 28 (82.4%) of the RAAs, and slight changes were found in the other six (17.6%). Again, no ruptures were found during follow-up.[36]

Morita et al published an additional study with similar results. They followed 30 patients for a median follow up of 69 months with conservative management only. At the end of the study, only two patients showed growth in their aneurysm, and only two other patients required an increase in blood pressure medications.[37]


Hypertension is the most common symptom found in RAA, with a reported incidence as high as 90%. Often, renal artery stenosis is associated with a poststenotic fusiform aneurysm. In this case, the hypertension can be attributed to the renal artery stenosis and activation of the renin-angiotensin system, with increased angiotensin II levels resulting in fluid retention and vasoconstriction.[23]

Hypertension in RAA without renal artery stenosis is not as well understood. Possible causes of hypertension in these cases may be related to renal ischemia secondary to thromboembolization distal to the aneurysm; in cases of large aneurysms, anatomic kinking of the renal artery has been reported.[38] Saccular and intrarenal aneurysms are less likely to be associated with hypertension.

In case series, 8-25% of patients presented with abdominal pain.[8, 11, 13] Patients with RAAs caused by dissection may present with flank pain, though most of those with spontaneous dissections are asymptomatic. New or worsening pain may also be indicative of a rapidly expanding aneurysm or impending rupture.

Hematuria may be another manifestation of dissecting RAA. Intraparenchymal aneurysms, which rupture into the collecting system, may also manifest as hematuria.

Collecting system obstruction is a rare presentation but has been documented in patients with larger aneurysms.

Renal infarction may be visualized on CT and is the result of embolization from the aneurysm sac.

Fewer than 3% of patients with RAAs experience a rupture.[6] Patients with RAA rupture typically have signs and symptoms of an abdominal catastrophe and may be in frank shock.[10]



Laboratory Studies

The following studies should be performed before any surgical intervention for a renal artery aneurysm (RAA):

  • Complete blood count (CBC)
  • Chemistry panel
  • Coagulation profile
  • Urinalysis 

Special attention should be paid to the blood urea nitrogen (BUN) and creatinine levels because these values are indicative of renal function and can be followed to confirm that no renal damage exists if the decision is made to manage an RAA nonoperatively.

In a patient with hypertension, RAA, and no renal artery stenosis, studies should be ordered to exclude other endocrine sources of hypertension, including the following:

  • Pheochromocytoma - 24-hour urine collection for vanillylmandelic acid, metanephrine, and normetanephrine
  • Primary aldosteronism - Serum potassium
  • Cushing syndrome - Cortisol levels
  • Carcinoid - Urinary 5-hydroxyindoleacetic acid

Imaging Studies

Because most RAAs are asymptomatic and are found incidentally during a workup for other intra-abdominal pathology, imaging studies are required only for preintervention planning or longitudinal follow-up care.


Ultrasonography (US) with duplex examination is the least invasive imaging study.[39] Two-dimensional (2D) US forms an anatomic picture based on the time delay of ultrasonic pulses reflected from structures. Vessel walls reflect ultrasound waves and appear white; blood absorbs and scatters ultrasound waves, appearing black. Normal vessels appear as dark-filled, white-walled structures.

Duplex studies use Doppler-shift measurement to detect the direction and velocity of blood flow. This can be useful in identifying renal artery stenosis. US can also be used in determining the how functional a kidney is by measuring its size. It should be kept in mind that the quality of imaging is highly operator-dependent and may be limited by the patient's body habitus.

Computed tomography

Computed tomography (CT) is the most widely available and reproducible imaging modality. It is the test of choice for diagnosis and follow-up. Its anatomic resolution is superior to that of US (see the image below).

(A) Computed tomography scan and (B) arteriogram o (A) Computed tomography scan and (B) arteriogram of the same patient with a saccular left renal artery aneurysm at a segmental renal artery branch.

The advent of CT angiography (CTA) and three-dimensional (3D) reconstruction has facilitated accurate preinterventional planning. Because intravenous (IV) iodinated dye must be used, the only real limitation of this modality is in patients who have a life-threatening dye allergy or impaired renal function. Non-life-threatening dye allergies can be managed with premedication with diphenhydramine (histamine-1 receptor antagonist), cimetidine (histamine-2 receptor antagonist), and methylprednisolone sodium succinate (glucocorticoid).

Magnetic resonance angiography

Magnetic resonance angiography (MRA) with gadolinium enhancement and 3D reconstruction can produce images similar in quality to those obtained with arteriography (see the image below). However, this technology is not as readily available as US or CT, and it is more expensive.[40]

Magnetic resonance imaging of a patient with 2 lef Magnetic resonance imaging of a patient with 2 left renal artery aneurysms. Both are saccular, one is at a segmental branch (closed arrow) and the other is intrarenal (open arrow). Of note: this patient also has a congenital absence of the right kidney.


Arteriography is the most invasive test but can be useful for helping define unclear anatomy seen on prior examinations (see the images below). For the most part, arteriography as a diagnostic test has been supplanted by CTA and MRA.

(A) Aortogram with calcified left renal artery ane (A) Aortogram with calcified left renal artery aneurysm (RAA). (B-C) Same RAA in magnified view, demonstrating the RAA is saccular, arising from the main renal artery.
(A) Computed tomography scan and (B) arteriogram o (A) Computed tomography scan and (B) arteriogram of the same patient with a saccular left renal artery aneurysm at a segmental renal artery branch.


Approach Considerations

Indications for intervention in patients with a renal artery aneurysm (RAA) include the following[20, 8, 13, 14] :

  • Rupture
  • Symptomatic RAA - Hypertension (from associated renal artery stenosis, refractory to medical management), pain, renal ischemia or infarction secondary to embolization from the aneurysm sac
  • RAAs in females who are pregnant or are contemplating pregnancy
  • Diameter greater than 2 cm
  • Enlarging RAA
  • RAA associated with acute dissection

Currently, there is no consensus regarding the size at which an RAA should be repaired in an asymptomatic patient. Experts have recommended RAA repair at diameters ranging from 1.5 to 3 cm,[8] though most suggest 2 cm.  Some reports have even suggest that larger asymptomatic saccular aneurysms may be managed expectantly. It should be noted that aneurysm rupture at a diameter of 1.5 cm has been reported.

Complete calcification of the wall of the aneurysm sac manifests in about 40% of patients. Such calcification was once believed to confer protection against rupture[21] ; however, this belief has since been questioned.[30, 41]

Asymptomatic small (< 2 cm in diameter) RAAs do not usually require treatment. One notable exception is an RAA in a woman who is pregnant or contemplating pregnancy. In view of the increased risk of rupture in such cases,[42] even small asymptomatic aneurysms should be repaired in this population.

For diagnosis and preinterventional planning, gadolinium-enhanced magnetic resonance angiography (MRA) and computed tomography (CT) angiography (CTA) with three-dimensional (3D) reconstruction have essentially replaced conventional arteriography.

Regular follow-up examination with ultrasonography (US) or CT is recommended in patients who are treated expectantly. Spontaneous cure by thrombosis of small aneurysms has been described.

Further refinements in endovascular techniques may allow more RAAs to be treated in this manner. Excellent short- and intermediate-term results have been described in the literature.[43, 44]

Case reports have described the use of robot-assisted laparoscopic approaches to the treatment of RAAs.[45, 46, 47, 48, 49]

Surgical Therapy

Emergency surgical repair of ruptured aneurysm

Emergency surgery is required to control hemorrhage and prevent death from a ruptured RAA. A midline approach with supraceliac aortic control is required because exposure of the renal vessels may be difficult in the presence of a large perinephric hematoma. The aortic cross-clamp can be removed once the renal artery is controlled.

In most cases of rupture, renal salvage may not be possible because of hemodynamic instability; therefore, nephrectomy may be necessary. In a hemodynamically stable patient, renal salvage with renal artery reconstruction may be considered.[23]

Management of the gravid uterus in a pregnant patient with acute RAA rupture should follow the same principles observed in treating hemorrhage caused by intra-abdominal trauma in a pregnant patient. Cesarean delivery should be avoided if possible because it increases operating time and results in additional blood loss.

Specific indications for cesarean delivery at the time of emergency laparotomy include interference of the gravid uterus with adequate exposure, fetal distress that outweighs the risk of fetal prematurity, and impending or recent maternal death.[50, 33]

Elective open repair

Elective repair of an RAA is generally undertaken to obviate the risk of rupture or treat the symptoms from RAA. Various operations are available for patients; the morphology and anatomic location of the aneurysm determine which approach to use. At times, partial nephrectomy may be needed, but with improved surgical technique, renal preservation is now the standard of care.

Tangential excision with primary repair or patch angioplasty

This is the procedure of choice for solitary saccular aneurysm at a proximal bifurcation and should be performed whenever feasible. It is associated with good anatomic and clinical results. Approximately one third of RAAs are amenable to such treatment. Aneurysms with small necks may be repaired primarily; otherwise, a patch angioplasty using autogenous saphenous vein or prosthetic material may be needed (see the image below).[20, 8]

(A) Extraparenchymal saccular aneurysm. (B) Tangen (A) Extraparenchymal saccular aneurysm. (B) Tangential excision with patch angioplasty.

Aneurysm excision with reconstruction using bypass

This is indicated if excision of the aneurysm and patch angioplasty is not possible. Fusiform aneurysm, large aneurysms, and aneurysms associated with proximal renal artery stenosis or fibromuscular dysplasia (FMD) are usually repaired in this manner.

After segmental excision of the aneurysm and renal artery, the preferred arterial reconstruction is with an autogenous saphenous vein aortorenal bypass graft. This is typically constructed with an end-to-side configuration for the proximal anastomosis and an end-to-end configuration for the distal anastomosis (see the image below).[20, 15] Saphenous vein graft and prosthetic material are both acceptable options, though saphenous vein graft is preferred because of its superior patency rates.[8]

(A) Fibromuscular dysplasia with string-of-beads a (A) Fibromuscular dysplasia with string-of-beads appearance and wide-necked extraparenchymal saccular aneurysm. (B) Aneurysm excision with reconstruction using a bypass graft.

If the aorta is heavily diseased by atherosclerosis, alternative bypass donor arteries may be used. These include splenorenal bypass, hepatorenal bypass, and iliac-to-renal bypass.

Extracorporeal vascular reconstruction with autotransplantation

With complex hilar or intrarenal aneurysms involving multiple arterial segments, in-situ exposure of the renal hilum is difficult. Extracorporeal or ex-vivo surgery allows adequate exposure.[51, 52] The renal artery and vein are divided to facilitate elevation of the kidney from the renal fossa onto the abdominal wall.

Simple continuous perfusion of the kidney via the renal artery with a cold (4°C) preservative solution such as that used in kidney transplantation allows the kidney to be maintained ex vivo for an extended time. Surface hypothermia is also maintained with a constant drip of chilled solution onto the kidney wrapped in an iced laparotomy pad.[7, 8, 15]

Once ex-vivo reconstruction with saphenous vein is complete, the kidney may be autotransplanted[53] into the iliac fossa, as in renal transplant recipients, or may be placed into the original renal fossa and revascularized by attaching the arterial graft to the aorta and the renal vein to the vena cava or renal vein remnant.

Autotransplantation into the renal fossa is favored over autotransplantation into the iliac fossa because many ex-vivo procedures are performed in relatively young patients. The iliac arterial system is susceptible to significant atherosclerotic disease, and attachment of the kidney there may adversely affect the long-term success of renovascular reconstruction.[7]

As a consequence of the complex nature of repairs at the hilum, there can be up to 45 minutes of warm ischemia time. Making the determination that ex-vivo repair will be needed before surgery is important. If not, considerable warm ischemia time may accumulate while in-situ repair is being attempted, thus dooming the eventual ex-vivo repair to failure.

The advantages of extracorporeal reconstruction include a superficial blood-free operating field and the possibility of needing an operating microscope.


Nephrectomy is often needed to treat intrarenal aneurysms because these commonly are not amenable to other repair techniques, except possibly coil embolization.

Partial nephrectomy may be combined with RAA repair in certain scenarios, as follows:

  • Multiple RAAs in both intraparenchymal and extraparenchymal location
  • RAA with associated renal lesions (malignancy or tumors)

Total nephrectomy is indicated in patients with the following conditions:

  • Multiple large intrarenal aneurysms that are not amenable to partial nephrectomy
  • RAA with associated renal lesions that are not amenable to partial nephrectomy
  • Aneurysmal rupture in a patient with shock who cannot tolerate the operating time needed for renal artery reconstruction
  • RAA in a nonfunctional kidney (as in severe ischemic renal atrophy or end-stage renal disease)
  • Prior failed revascularizations [5, 33]

Minimally invasive surgery

Laparoscopic RAA repair with robotic assistance has been described.[48, 49]  Such an approach may be considered as an alternative to open surgical repair when endovascular treatment is not an option.

Operative details

Once a patient is deemed a candidate for surgery, appropriate preparations are needed. At a minimum, all patients should have a complete blood count (CBC), chemistry panel, coagulation profile, urinalysis, and blood cross-match for 2 units. Patients older than 35 years should undergo electrocardiography (ECG) and be appropriately screened and evaluated for cardiac disease prior to elective surgery. Patients who are older than 50 years or have a history of pulmonary disease should undergo preoperative chest radiography.

Depending on the planned procedure, the patient should be positioned for either a transperitoneal or a retroperitoneal approach. In most cases, a retroperitoneal incision provides adequate exposure for the renal artery and ex-vivo repairs. A transperitoneal incision is indicated mainly for ruptured RAAs, but this incision requires bowel manipulation, causing postoperative ileus. This is minimized with a retroperitoneal incision.[33]

As with all aneurysm surgery, the principles of carefully obtaining proximal and distal control before dissecting around the aneurysm are essential. If a complex repair is anticipated, early consideration should be given to performing an ex-vivo reconstruction.

Endovascular Therapy

Advances in endovascular techniques have led investigators to attempt endovascular therapy for visceral aneurysms, including RAAs.[26, 54, 55, 56, 57]  Cases have been reported where endovascular approaches have been applied to ruptured RAAs; however, larger studies are required to evaluate long-term outcomes.[58]

Although the clinical and angiographic success rates using these techniques are very high, the long-term results are not yet well defined. Periodic surveillance for patients treated with endovascular techniques is essential.

Coil embolization

Coils are thin platinum or steel wires with retained memory that allows them to coil once deployed from a catheter. They cause a disturbance of blood flow with subsequent thrombosis (see the first image below). With the advent of microcoils and more flexible delivery catheters, coil embolization is being used more often,[12]  but potential disadvantages still exist. If the entire aneurysm sac is not filled with coils, the aneurysm will continue to expand (see the second image below).

Arteriogram of saccular renal artery aneurysm afte Arteriogram of saccular renal artery aneurysm after coil embolization.
Subsequent expansion of aneurysm 6 months after co Subsequent expansion of aneurysm 6 months after coil embolization.

Originally, only saccular aneurysms with small necks were filled with coils because of the fear of coil migration. Subsequently, investigators began to treat wide-necked saccular aneurysms by placing a bare-metal stent across the neck, then filling the aneurysm with coils through the interstices of the stent.[59, 60]  One last advantage of coil embolization is that it can be used in extraparenchymal or intrarenal aneurysms.[61]

Liquid embolization

An alternative technique uses ethylene vinyl alcohol copolymer as a liquid embolization agent. While placing an inflated angioplasty balloon in the main renal artery for protection, the operator is able to infuse the polymer directly in the aneurysm sac in a controlled manner under visualization. One of the advantages of this method is that it can be used to provide precise treatment for wide-neck RAAs.[62]

Stent graft

Stent grafts are bare-metal stents lined with polytetrafluoroethylene (PTFE) or Gore-Tex. They were originally handmade, but devices with greater flexibility and lower profiles were subsequently developed.[63]  Stent grafts require a length of nondilated artery proximal and distal to the aneurysm in order to form a seal and exclude the aneurysm from circulation. They are of limited utility at renal artery bifurcations but can be used in fusiform or saccular aneurysms more proximally located in the main renal artery. An additional benefit is the ability to treat both renal artery stenosis and RAA (see the image below).[64, 65]

(A) Renal artery stenosis with poststenotic fusifo (A) Renal artery stenosis with poststenotic fusiform aneurysm. (B) Exclusion of aneurysm and dilatation of stenosis with endovascular stent graft.

Postoperative Care

Postoperatively, attention should be paid to a patient’s renal function (with urine output) and chemistries. Otherwise, standard principles of postoperative care should be applied.


Aside from the usual complications that may accompany any major abdominal surgical procedure, the complications inherent in RAA surgery include the following:

  • Native renal artery or graft occlusion in the early postoperative period, most often due to technical error
  • Diminished renal function due to prolonged warm ischemia time
  • Greater risk of postoperative cardiac events due to the high prevalence of atherosclerotic disease in this group of patients
  • Postoperative graft occlusion due to technical error, the prothrombotic nature of some graft material, or hypercoagulability from a variety of sources
  • Segmental ischemia of the kidney from occlusion of a branch vessel by emboli during open repair, coil migration, or incorrect stent graft placement
  • In the case of endovascular repair, possible continued aneurysmal expansion from inadequate embolization or seal after stent placement

Barrionuevo et al performed a systematic review and meta-analysis of studies involving the management of visceral artery aneurysms, which included 1279 RAAs.[66]  For RAAs, they reported a postembolization syndrome rate of 9% and a coil migration rate of 29%; otherwise, access-site complication rates were low.

Long-Term Monitoring

Ideally, patients should have yearly postoperative renal artery duplex US scanning to monitor the patency of arterial reconstruction and identify new aneurysms. Abnormal findings on duplex US can be confirmed by performing CT, MRA, or conventional arteriography. Those who have undergone endovascular repair merit close follow-up because long-term data on the success of this approach are limited.[67, 43]