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Classification:
RAAs can be classified as extraparenchymal (saccular, fusiform, false/dissecting) or intraparenchymal.
Extraparenchymal
- Saccular/fusiform type - Fibromuscular dysplasia (FMD), Kawasaki disease
- False/dissecting type - Blunt abdominal trauma, intraluminal catheter–induced injury, spontaneous
Intraparenchymal
- Polyarteritis nodosa
- Tuberculosis
- Neurofibromatosis
- Mycotic
- Ehlers-Danlos syndrome
Pathophysiology:
Regardless of etiology, the common factor in the pathogenesis of RAA is compromise of one or more layers of the vessel wall. Common to saccular and fusiform aneurysms are degenerative fibroplasia-type changes in the media associated with FMD. Although atherosclerotic changes are often observed in the aneurysm wall, this is believed to be secondary.
Two theories are proposed to explain renal artery injury after blunt trauma. The first relates to sudden anterior displacement of the relatively mobile kidneys with rapid deceleration. The resultant tension generated in the vascular pedicle causes fracture of the intima, predisposing it to subintimal dissection. The second mechanism involves direct arterial wall contusion against the vertebral bodies.
Intraparenchymal aneurysms are believed to arise primarily from inflammatory changes of the vessel wall. These commonly develop into microaneurysms.
Although pregnancy is not associated with an increased incidence of aneurysm 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.
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.
Clinical:
Asymptomatic
Most RAAs are asymptomatic and are found incidentally while investigating other intra-abdominal pathologies using diagnostic imaging studies such as computed tomography (CT), duplex ultrasonography, angiography, magnetic resonance imaging (MRI), or magnetic resonance angiography (MRA).
Hypertension
The incidence rate of hypertension in patients with RAAs may be as high as 90%. The association between significant renal artery stenosis causing poststenotic fusiform aneurysm and hypertension can be attributed to activation of the renin-angiotensin system, with increased angiotensin II levels resulting in fluid retention and vasoconstriction. In the presence of a normal contralateral kidney, a compensatory pressure–induced natriuresis occurs to offset the volume expansion. However, the actions of angiotensin II on neurogenic mechanisms and vascular endothelium may be of foremost importance in accounting for the persistence of hypertension. Hypertension associated with saccular-type aneurysms is not as well understood, although renal ischemia has been reported from thromboembolization distal to the aneurysm.
Flank pain
Patients with RAAs caused by dissection may present with flank pain, although most of those with spontaneous dissections are asymptomatic.
Hematuria
Hematuria may be another manifestation of dissecting RAA. Intraparenchymal aneurysms, which rupture into the collecting system, may also manifest as hematuria.
Collecting system obstruction
Collecting system obstruction is a rare presentation but has been documented in patients with larger aneurysms.
Renal infarction
Renal infarction may be visualized on CT scan images and is the result of embolization from the aneurysm sac.
Rupture
Patients do not usually present with rupture. Patients with RAA rupture typically have signs and symptoms of an abdominal catastrophe and may be in frank shock.
The renal arteries deliver to the kidneys of a normal person at rest 1.2 litres of blood per minute, a volume equivalent to approximately one-quarter of the heart’s output. Thus, a volume of blood equal to all that found in the body of an adult human being is processed by the kidneys once every four to five minutes. Although some physical conditions can inhibit blood flow, there are certain self-regulatory mechanisms inherent to the arteries of the kidney that allow some adaptation to stress. When the total body blood pressure rises or drops, sensory receptors of the nervous system located in the smooth muscle wall of the arteries are affected by the pressure changes, and, to compensate for the blood pressure variations, the arteries either expand or contract to keep a constant volume of blood flow.
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