Discussion
Renal artery aneurysms are uncommon, with an estimated incidence of 0.09% in the general population, 0.1%–2.5% in angiographic series, and up to 9.7% in autopsy series. [3] They constitute between 15 and 25% of all visceral artery aneurysms, second only to splenic artery aneurysms, and are most commonly located along the main renal artery. [3, 6] They are bilateral in 10% of cases. [2]
Renal artery aneurysms exhibit calcification in 18% of cases and only 8.5% are larger than 20 mm. [3] The largest aneurysm we found in the literature measured 25 cm. [7] They may be true (saccular and fusiform), false (arising from penetrating or blunt trauma) or dissecting. [2] Approximately 75% of the renal artery aneurysms are saccular and almost invariably occur at the main renal artery bifurcation. [2] Only 10% are intraparenchymal, usually cortical and associated with polyarteritis nodosa. [2]
Peak incidence occurs between the ages of 40-60 years and some authors report it to be equal between men and women, while others report a higher incidence in women. [2, 3, 6]
The two most common underlying aetiologies are atherosclerosis or fibrous dysplasia, renal angiomyolipoma and congenital renal malformations being much less frequent causes. [3, 4] Secondary renal artery aneurysms are seen in such conditions as malignancies, infection (mycotic), and trauma, in association with systemic diseases, such as polyarteritis nodosa, neurofibromatosis, William’s syndrome, midaortic syndrome, autoimmune vasculitis, and tuberous sclerosis, or are iatrogenic (e.g. renal biopsy). [2]
The clinical significance of these aneurysms varies from that of an incidental finding to hypertension, flank pain and haematuria. [3]
Possible complications include:
. Rupture, with a generally low estimated risk (between 2,8 and 5,6%), thought to be greater during pregnancy, in patients with polyarteritis nodosa and in non-calcified aneurysms, with reported mortality rates above 80%; [1, 3, 4]
. Embolisation; [1]
. Hypertension, which has no relation with renal artery stenosis and has a prevalence of up to 80%. Hypotheses regarding the pathophysiologic basis of hypertension include coexisting renal artery stenosis, microembolisation from the aneurysm, compression or kinking of the renal artery or its branches, and turbulent flow; [1, 6]
. Renal insufficiency; [1]
Plain film findings include marginal calcifications of the aneurysm and distended bowel loops as a sign of retroperitoneal irritation. Ultrasound may demonstrate a distended pelvis and perirenal collections in cases of rupture but findings are otherwise generally non-specific. MDCT Angiography is the preferred imaging modality due to its unique spatial resolution. [4]
Follow-up of aneurysms < 2 cm is generally accepted. [6] Standard treatment for larger aneurysms is surgery and includes aneurysm resection, aortorenal bypass, reno-renal interposition, reimplantation, patch angioplasty, and nephrectomy. [3] Endovascular treatment is nowadays considered to be a valid alternative and includes both coil embolisation and endoprothesis placement, but no direct comparison studies are available. [1]
Indications for treatment include rupture, renovascular hypertension, embolisation, dissection, aneurysm expansion, size >= 1.5 cm to >= 2.5 cm, pregnancy and child bearing age. [3]
