Other Renal Artery Diseases
Renal Arterial Aneurysms
A renal arterial aneurysm is a localized dilatation of the main renal artery or its branches or both caused by weakening of the elastic tissue and media of the arterial wall. The estimated incidence of such lesions in the general population ranges from 0.09% to 0.3%. Renal arterial aneurysms may be clinically significant because of a causative relation to hypertension, associated local symptoms, or the risk of catastrophic rupture in certain situations (Novick, 1982). According to the classification of Poutasse (1975), there are four basic types of renal artery aneurysms: saccular, fusiform, dissecting, and intrarenal (Fig. 39–17).
Figure 39–17 Selective renal arteriograms demonstrate the four types of renal artery aneurysms. A, Saccular aneurysm located at the bifurcation of the main renal artery. B, Fusiform aneurysm distal to a stenotic lesion of the main renal artery. C, Dissecting aneurysm involving a renal artery branch. D, Intrarenal aneurysm.
Saccular aneurysms are the most common type and constitute about 75% of renal artery aneurysms. They generally occur at the bifurcation of the renal artery, perhaps owing to an inherent weakness in the wall of the artery at this point. Because of this location, branch arterial involvement is common. The incidence of bilateral or multiple aneurysms or both is approximately 25%. These aneurysms may become involved with secondary atherosclerotic degeneration or intramural calcification or both. Incompletely calcified aneurysms may become soft, thin, and ulcerated between zones of calcification, thus predisposing to rupture. In addition to rupturing spontaneously, saccular aneurysms may erode into the renal vein or into the renal pelvis. Mural thrombus formation may also occur within saccular aneurysms, occasionally leading to peripheral renal embolization.
Fusiform aneurysms occur as a uniform dilatation of an entire segment of the renal artery to as much as three to four times its normal diameter. These aneurysms range in length from 1 to 3 cm and are generally not calcified. They are typically found in young hypertensive patients with stenosing fibrous renal arterial disease. The fusiform aneurysm is actually a poststenotic dilatation and can involve either the main renal artery or its branches. The major complication of this lesion is thrombosis of the involved arterial segment from progressive proximal stenosing vascular disease.
A dissecting aneurysm results from a tear in the internal elastic membrane of the renal artery, and as blood flows through the opening, the intima is separated from the remainder of the arterial wall. In some patients, the dissection may reenter the lumen distally to preserve renal function. In other cases, arterial thrombosis with renal infarction or rupture with hemorrhage may occur. Dissecting aneurysms are most often complications of renal arterial involvement with atherosclerosis, intimal fibroplasia, or perimedial fibroplasia. Less commonly, such an aneurysm may occur as an extension of a dissecting aortic aneurysm.
Intrarenal arterial aneurysms are of mixed origin and may be congenital, post-traumatic, iatrogenic, neoplastic, or associated with polyarteritis nodosa. They are usually saccular or fusiform and may or may not be calcified. Intrarenal aneurysms constitute approximately 17% of all renal arterial aneurysms, and they do have the propensity for rupture. Intrarenal aneurysms that occur after blunt trauma or closed renal biopsy occasionally resolve spontaneously with expectant management.
In general, the diagnosis of renal arterial aneurysm should be considered when ringlike calcification in or near the renal hilum is found on a plain abdominal radiograph. These calcifications occur in about 50% of cases. The majority of renal arterial aneurysms are small and asymptomatic. The most common clinical manifestations are hypertension, subcostal or flank pain, hematuria, an abdominal bruit, and, rarely, a palpable pulsating mass. RVH is reported to occur in 15% to 75% of patients and may be due to turbulent flow within an aneurysm, associated arterial stenosis, dissection, arteriovenous fistula formation, thromboembolism, or compression of adjacent arterial branches by a large aneurysm. Complications of renal arterial aneurysms include peripheral dissection, arterial thrombosis with renal infarction, emboli arising from mural thrombus within an aneurysm, obstructive uropathy, erosion into a vein with formation of an arteriovenous fistula, and spontaneous rupture with hemorrhage. Factors that appear to predispose to aneurysmal rupture include absent or incomplete calcification, aneurysmal size greater than 2 cm in diameter, coexisting hypertension, and pregnancy.
A small (2-cm) well-calcified renal arterial aneurysm in an asymptomatic normotensive patient does not require operative intervention. These aneurysms can be followed with serial plain abdominal radiographs to detect any change in size. Surgical removal is indicated for renal arterial aneurysms, regardless of size, in (1) aneurysm causing renal ischemia and hypertension, (2) dissecting aneurysm, (3) aneurysm associated with local symptoms such as flank pain or hematuria, (4) aneurysm occurring in a woman of child-bearing age who is likely to conceive, (5) aneurysm occurring with functionally significant renal arterial stenosis, (6) aneurysm with radiographic evidence of expansion on serial radiographs, or (7) aneurysm containing a thrombus detectable on angiography with evidence of distal embolization.
When none of these criteria are present, small (2-cm) asymptomatic noncalcified or incompletely calcified aneurysms can be managed nonoperatively. Such patients should be followed periodically with serial CT or MRI studies to document the size of the aneurysm. It is not possible to rigidly define indications for operative intervention in asymptomatic patients with aneurysms greater than 2 cm in diameter and with none of the previous criteria. The available data would seem to support surgical excision, if these aneurysms are not calcified throughout or are intrarenal because of the increased tendency to rupture in these settings.
In the largest series of renal artery surgery reported in the recent literature (Henke et al, 2001), a total of 121 patients underwent surgical repair. Eight unplanned nephrectomies were necessary resulting in the need for permanent dialysis in one patient, no perioperative mortality was encountered, and all but two reconstructions remained patent at follow-up.
In a retrospective review of surgical repair of renal artery aneurysms in 94 patients, Pfeiffer and colleagues (2003) encountered one postoperative mortality (in an emergency repair secondary to aneurysm rupture), overall morbidity of 17%, and a primary success rate of 97%.
English and colleagues (2004) reported their results of surgical repair of 72 renal artery aneurysms of varying etiology over a 16-year period. Only one aneurysm was deemed not reconstructable, and nephrectomy was performed. One operative mortality was encountered, and 12% of patients had significant perioperative morbidity, with 96% of repairs maintaining patency at 48 months.
A significant body of literature (almost all case reports) has accumulated over the last few years reporting successful endovascular management of renal artery aneurysms as well as dissection of the renal artery. In the case of renal artery aneurysms, two methods of endovascular treatment are reported. The first involves embolization of the aneurysm (usually with coils) to occlude it without disrupting the renal blood flow (Halloul et al, 2000; Karkos et al, 2000; Mounayer et al, 2000; Tshomba et al, 2002; Lupattelli et al, 2003). The second method involves placing an arterial stent in the renal artery or the branch where the aneurysm originates, thereby maintaining flow through the stent and effectively excluding the aneurysm (Tan et al, 2001; Bruce and Kuan, 2002; Pershad and Heuser, 2004). Stenting the renal artery across an aneurysm has also been described as a successful and rapid method of dealing with ruptured renal artery aneurysm (Schneidereit et al, 2003). Dissection of the renal artery also can be managed endovascularly by placing a renal artery stent through the area of dissection to keep the lumen patent and keep the dissected intima immobilized against the outer layers of the artery (Bilge et al, 2003).
Renal Arteriovenous Fistula
Renal arteriovenous fistulas are relatively uncommon lesions that are generally discovered during the course of angiographic evaluation for suspected renal or renovascular disease. There are three categories of renal arteriovenous fistulas: congenital, idiopathic, and acquired (Tynes et al, 1970; Novick, 1982).
Congenital fistulas have a cirsoid or angiomatous configuration with multiple communications between arteries and veins. They are usually supplied by a renal arterial branch of normal caliber. The angiographic appearance is one of multiple, small, interconnecting arterial and venous channels with impaired distal renal parenchymal vascularity and early filling of the renal vein. They constitute 22% to 25% of all renal arteriovenous fistulas, occur equally in both sexes, and generally do not become manifest until adult life.
Idiopathic fistulas are single, are not cirsoid, and have no apparent cause. They constitute only 3% to 5% of all renal arteriovenous fistulas. These lesions are called idiopathic because their angiographic appearance is similar to that of acquired arteriovenous fistulas, but their origin is unclear.
Acquired fistulas are the most common type, accounting for 70% to 75% of all renal arteriovenous fistulas. On angiography, they appear as solitary communications between an artery and a vein. By far the most common cause is iatrogenic trauma resulting from needle biopsy of the kidney (Fig. 39–18). Other causes include renal carcinoma, blunt or penetrating renal trauma, inflammation, and renal surgery such as nephrectomy, partial nephrectomy, or nephrolithotomy.
Figure 39–18 Left renal arteriogram shows renal arteriovenous fistula with early filling of the renal vein. This patient had previously undergone needle biopsy of the left kidney.
The clinical manifestations of a renal arteriovenous fistula depend on the size of the fistula. Approximately 75% of patients have an abdominal bruit, which is usually loud, high pitched, and continuous with systolic accentuation. Congestive heart failure, cardiomegaly, and diastolic hypertension are observed in 50% of patients. Hematuria is present in about one third of cases, tachycardia is occasionally found, and a palpable flank mass from spontaneous rupture is rarely encountered.
The management of a patient with a renal arteriovenous fistula depends on the cause of the fistula and the associated clinical manifestations. For patients with renal carcinoma, immediate nephrectomy is obviously indicated. Approximately 70% of fistulas occurring after needle biopsy of the kidney close spontaneously within 18 months. A smaller number of fistulas diagnosed immediately after renal trauma have also resolved spontaneously. Therefore in the absence of significant related symptoms, expectant management is appropriate initially in these cases.
Treatment of renal arteriovenous fistulas is indicated for patients who have hypertension, heart failure, severe hematuria, serial angiographic evidence of an expanding lesion, rupture, or progressive renal failure. When specific therapy of these lesions is indicated, renal-sparing procedures should be employed whenever possible.
Transcatheter angiographic occlusion is a nonsurgical therapeutic alternative that has been employed primarily in treating patients with postbiopsy fistulas, in which the arteriovenous connecting vessels are usually small. More recently, transcatheter occlusion of congenital or idiopathic fistulas with a stainless steel coil has also been performed.
Various operations have been employed in the surgical treatment of renal arteriovenous fistulas. Most congenital or cirsoid fistulas have been managed with total or partial nephrectomy, because of the difficulty of completely excising the many small communicating vessels. In patients with idiopathic or acquired fistulas, a single communication between the artery and the vein is characteristically present, and surgical obliteration of the fistula with preservation of the involved kidney is more often possible.
Renal Artery Thrombosis or Embolism
Thromboembolic disorders of the renal artery can present as fulminant clinical syndromes that threaten life or may be entirely asymptomatic and detected only at postmortem examination (Hoxie and Coggins, 1940; Schoenbaum et al, 1971). The various causes of acute renal artery thrombosis or embolism are listed in Table 39–14. The term paradoxical embolism refers to a clot originating in the venous circulation that gains entrance to the systemic arterial circulation through an intracardiac septal defect.
Table 39–14 Causes of Renal Arterial Thrombosis and Embolism
| Renal Artery Thrombosis |
| Renal Artery Embolism |
Renal arterial thrombosis commonly involves the proximal or middle third of the main renal artery, whereas renal arterial embolization generally involves peripheral arterial branches. Acute arterial occlusion is more common on the left side because of the more acute angle between the left renal artery and the aorta. Post-traumatic renal arterial occlusion is also more common on the left side, presumably because of the acute angulation of the shorter left renal artery at its aortic junction, which predisposes to intimal disruption with deceleration of the mobile kidney.
The clinical symptomatology in these disorders is extremely varied. Bilateral acute renal arterial occlusion presents with rapidly progressing oliguric renal failure, whereas chronic occlusion of a single renal artery may be unnoticed because of the development of collateral circulation. The most common symptoms, when present, are dull, aching abdominal or flank pain often associated with nausea, vomiting, and fever. Other findings include hypertension, albuminuria, microscopic hematuria, leukocytosis, and elevation of serum lactate dehydrogenase levels.
Patients with unilateral renal arterial embolic occlusion generally have serious underlying extrarenal disease and are best managed nonoperatively with systemic anticoagulation or by percutaneous transcatheter thromboembolectomy (Millan et al, 1978; Hamilton, 1996). Patients with unilateral traumatic renal arterial thrombosis also often have severe associated injuries, and the results of vascular reconstruction are generally unsatisfactory unless this is undertaken within several hours of the time of injury. Surgical treatment in these cases is generally ill advised when a normal contralateral kidney is present. Percutaneous intra-arterial infusion of a fibrinolytic agent, such as streptokinase, now offers a nonoperative approach to the management of acute renal arterial thrombosis (Hamilton, 1996).
Renovascular reconstruction is generally indicated when renal artery thrombosis or embolism occurs bilaterally or in a solitary kidney. Alternatively, if angiographic and isotopic studies in such cases demonstrate an extensive collateral vascular supply maintaining renal viability, an initial therapeutic trial with one of the previously mentioned nonoperative approaches may be worthwhile.
Neurofibromatosis
Neurofibromatosis affecting the renal arteries is a congenital hereditary disorder characterized by café-au-lait cutaneous pigmentation, cutaneous neurofibromas, tumors of the CNS, skeletal disorders, and occasional gigantism (Grad and Rance, 1972; Tilford and Kelsch, 1973). Hypertension in patients with neurofibromatosis is most often due to renal artery stenosis; less commonly, this may be the result of an associated pheochromocytoma or aortic coarctation. Vascular abnormality occurs in the kidneys, heart, and gastrointestinal tract and consists of fibrosis and thickening of the intima, proliferation of neural tissue within the arterial wall, perivascular nodular proliferations, and occasional aneurysmal dilatation. In the kidney, arterial stenosis usually occurs at the origin or in the proximal third of the main renal artery, and the angiographic appearance may be indistinguishable from that of intimal fibroplasia. Considering the young age of these patients, renal revascularization is generally the treatment of choice for associated RVH.
Middle Aortic Syndrome
The middle aortic syndrome is a rare disorder, occurring in children or young adults, characterized by nonspecific stenosing arteritis affecting the aorta and its major branches, including the renal arteries (Fig. 39–19). This is thought to be a form of Takayasu disease, and an autoimmune pathogenesis is suspected (Kaufman, 1973). This disease can extensively involve the subdiaphragmatic aorta or, in some cases, may spare the aorta and involve primarily the renal or splanchnic vessels. The natural history is not well understood because most cases are diagnosed when the disease has already resulted in significant renal arterial stenosis in young good-risk patients, thus necessitating early revascularization. Because the inflammatory process generally does not extend to involve the iliac arteries, renal autotransplantation is the surgical treatment of choice.
Extrinsic Obstruction
Extrinsic obstruction of the renal artery has been observed but is extremely rare (Silver and Clements, 1976). Neural tissue, musculocutaneous fibers, and diaphragmatic crura have been suggested as etiologic factors contributing to this process. Other possible causes of extrinsic perivascular fibrosis include inflammation, trauma, tumor, or prior radiation.
The Page Kidney
In 1934, Page (1939) produced a renin-dependent model of hypertension by wrapping a dog kidney in cellophane. Hypertension could be reversed by removing the cellophane wrap or the kidney. The clinical equivalent of this hypertensive model is the kidney compressed by a subcapsular or perirenal process causing renal ischemia, inducing unilateral hypersecretion of renin and contralateral suppression. Causes of the perinephric process include blunt trauma, closed renal biopsy, anticoagulation, or hemorrhage from a tumor.
The diagnosis of the Page kidney depends on the presence of either a surrounding hematoma or an encasing fibrous pseudocapsule. Imaging with ultrasonography, CT, or MRI localizes the hematoma or fibrous capsule.
The treatment of the Page kidney aims to preserve renal function and cure hypertension. Medical antihypertensive therapy plus observation, percutaneous evacuation of the perirenal hematoma, open drainage of the hematoma, and nephrectomy have all been used (Suffrin, 1975).
Some cases of the acute Page kidney with new-onset hypertension have spontaneously resolved. A hematoma may reabsorb, relieving the parenchymal compression without forming an adhesive fibrotic pseudocapsule. Treatment with medical antihypertensive therapy can control the blood pressure until the hematoma resolves. If the hematoma does not resolve, it may be drained percutaneously or surgically.
Renal Parenchymal Disease
Renin-mediated hypertension may be secondary to a variety of renal parenchymal diseases. The incidence of hypertension in patients with chronic pyelonephritis is approximately 5% to 10%. The mechanism of renin-mediated hypertension in such kidneys with segmental scars is ischemia of the relatively normal renal cortex in proximity to areas of interstitial fibrosis, within which are small vessels with intimal thickening. Other renal disorders that may cause hypertension include hydronephrosis, congenital hypoplasia or dysplasia, segmental hypoplasia (Ask-Upmark kidney), vesicoureteral reflux, renal cell carcinoma, benign cyst, Wilms tumor, radiation nephritis, or juxtaglomerular cell tumor.
Key Points: Management of Patients with Renal Artery Disease
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