(Radiographics. 2000;20:1321-1340.)
© RSNA, 2000
CT Evaluation of Renovascular Disease1
Akira Kawashima, MD ,
Carl M. Sandler, MD ,
Randy D. Ernst, MD,
Eric P. Tamm, MD,
Stanford M. Goldman, MD and
Elliot K. Fishman, MD
1 From the Departments of Radiology (A.K., C.M.S., R.D.E., E.P.T., S.M.G.) and Urology (C.M.S., S.M.G.), University of Texas Medical School, Houston; the Department of Radiology, Lyndon B. Johnson General Hospital, 5656 Kelley St, Houston, TX 77026 (A.K., C.M.S., R.D.E., S.M.G.); and the Russell H. Morgan Department of Radiology and Radiological Science, Johns Hopkins Medical Institutions, Baltimore, Md (E.K.F.). Recipient of a Certificate of Merit award for a scientific exhibit at the 1998 RSNA scientific assembly. Received May 3, 1999; revision requested July 13 and received May 1, 2000; accepted May 4. Address correspondence to A.K. (e-mail: akira.kawashima@uth.tmc.edu).
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Abstract
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Computed tomography (CT) plays an important role in evaluation and management of primary renovascular disease. Nonenhanced CT is useful for demonstrating renal hemorrhage, renal parenchymal or vascular calcifications, and masses. Contrast material–enhanced CT is essential to identify global or regional nephrographic abnormalities resulting from the vascular process (eg, renal infarcts, ischemia secondary to renal artery stenosis, arteriovenous communications). In addition, renal manifestations of a systemic disease (eg, vasculitis, thromboembolic disease) can be seen at CT. In trauma, occlusion of the main renal artery can be accurately diagnosed with contrast-enhanced CT. In cases of spontaneous renal hemorrhage without an apparent cause (eg, vasculitis, coagulopathy), a careful CT study should be performed to exclude renal cell carcinoma. The presence of fat in a hemorrhagic renal mass larger than 4 cm in diameter is characteristic of angiomyolipoma complicated by hemorrhage. Acute renal vein thrombosis appears as a clot in a distended renal vein, whereas renal vein retraction with collateral vessels is highly indicative of chronic thrombosis. Helical CT, especially with multiplanar two-dimensional and three-dimensional reconstruction following an intravenous injection of iodinated contrast material, has greatly improved our ability to directly image the proximal renal arteries and detect vascular lesions.
Index Terms: Aneurysm, renal, 81.73, 96.73 • Arteriovenous malformations, renal, 81.1494, 96.149 • Fistula, arteriovenous, 81.494, 96.494 • Kidney, hemorrhage, 81.367, 96.367 • Kidney, infarction, 81.77, 96.771 • Kidney, injuries, 81.48, 96.41 • Renal arteries, stenosis or obstruction, 961.72 • Renal veins, thrombosis, 81.751, 966.751 • Ureter, stenosis or obstruction, 821.844 • Vasculitis, 81.62, 96.62
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LEARNING OBJECTIVES FOR TEST 3
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After reading this article and taking the test, the reader will be able to:
- List the vascular conditions that involve the kidney.
- Identify the CT features of renovascular disease.
- Develop a management plan for each condition by integrating the imaging findings with clinical information.
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Introduction
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Computed tomography (CT) plays an important role in evaluation and management of both primary renovascular disease and the secondary manifestations of renovascular disease. In this article, CT techniques for evaluation of renovascular disease are described. A systematic review of renovascular disease is then presented, which is categorized according to the vascular, parenchymal, and perinephric CT manifestations and illustrates the key CT findings. The specific subjects discussed are renal trauma, arteriovenous communications, renal artery aneurysm, vasculitis, spontaneous renal hemorrhage, renal infarct, renal artery stenosis, secondary ureteropelvic junction (UPJ) obstruction, and renal vein thrombosis.
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CT Techniques
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Our current CT protocol for initial evaluation of the kidneys consists of both nonenhanced and contrast material–enhanced CT scans. A contrast-enhanced study is essential for evaluating patients with suspected renovascular disease. Nonenhanced CT is useful for demonstrating renal hemorrhage, renal parenchymal or vascular calcifications (calcification in the wall of an aneurysm, cortical nephrocalcinosis), and masses. In cases of trauma, nonenhanced CT is usually unnecessary. Fluid with high attenuation (40–90 HU) is most consistent with acute hemorrhage. Contrast-enhanced CT allows accurate localization of a renal hematoma in the intrarenal, subcapsular, perinephric, or paranephric space or any combination of these. At dynamic contrast-enhanced CT, active bleeding appears as patchy areas of very high attenuation (85–370 HU) within a high-attenuation hematoma (1).
A contrast-enhanced study can allow direct visualization of the renal vessels and identification of nephrographic abnormalities due to a renovascular process. A renal infarct can be accurately demonstrated following intravenous administration of contrast material. Delayed CT scans of the kidneys are necessary when a mass, infarct, or urinary obstruction is suspected on the early-phase scans.
Helical CT is preferred to conventional incremental CT for imaging the renal parenchyma and collecting system because fast volume acquisition can be performed during respiratory suspension following intravenous administration of a contrast material bolus with a mechanical injector (2,3). Helical CT can show a particular phase of the nephrographic progression, including the vascular, cortical nephrographic, diffuse nephrographic, and excretory phases (3,4). Identification of global or regional nephrographic abnormalities during a particular phase of enhancement is valuable in assessing renal perfusion and function (2). Renal vascularity is evaluated during the vascular phase, which occurs approximately 15–25 seconds after the start of intravenous contrast material administration. A hyperattenuating cortical nephrogram with corticomedullary differentiation is obtained during the cortical (corticomedullary differentiation) nephrographic phase, which occurs approximately 25–80 seconds after the start of intravenous contrast material administration (4). A homogeneous nephrogram can be obtained during the diffuse (parenchymal) nephrographic phase, which occurs approximately 85–120 seconds after the start of intravenous contrast material administration (4). Contrast material starts to appear in the collecting system in the excretory phase, which occurs approximately 3–5 minutes after the start of intravenous contrast material administration (4).
No standard acquisition techniques have been established for scanning the kidneys. Our current CT protocol for a dedicated kidney study includes an initial axial or helical nonenhanced scan of the kidneys with contiguous 5-mm-thick sections following a scout scan. Contrast-enhanced helical CT studies of the abdomen are performed within 30 seconds for the cortical nephrographic phase. Helical scans for the diffuse nephrographic phase are obtained approximately 100 seconds after the start of intravenous contrast material administration. When necessary, abdominal scans above the kidneys may be obtained before obtaining the nephrographic scans. Rapid injection of a 150-mL bolus of 60% nonionic iodinated contrast material (iohexol [iodine, 300 mg/mL]; Omnipaque 300, Nycomed Amersham, Princeton, NJ) can be performed at a rate of 2.0–3.0 mL/sec via the antecubital fossa by using a mechanical power injector and an 18–20-gauge angiographic catheter. The scanning parameters include a collimation of 5 mm, a pitch of 1.5, and an image reconstruction increment of 5 mm (CT/i HighSpeed; GE Medical Systems, Milwaukee, Wis). Scans through the kidneys should be obtained during one breath hold to maximize the advantage of a volume data set without misregistration. Optimal enhancement can be achieved by using an optional upgrade (SmartPrep; GE Medical Systems), which allows visual monitoring of the time-enhancement tracking curve by means of a series of very-low-milliamperage scans and region-of-interest measurements (5). The onset of the diffuse nephrographic phase occurs earlier at a higher rate of contrast material injection and is delayed in patients with compromised cardiac output (6). Excretory-phase CT scans are necessary when focal or diffuse nephrographic abnormalities and urinary obstruction are suspected.
Typical acquisition parameters for CT angiography of the renal artery include a collimation of 3 mm, a pitch of 1.5–2.0, a reconstruction interval of 1–2 mm, a scan delay of 25 seconds after the start of intravenous contrast material administration, and an injection rate of 3 mL/sec or greater (7–11). The preliminary bolus timing technique is also useful, particularly for evaluating patients with compromised cardiac output (7).
When the timing of the scan is optimized to the peak of intravascular enhancement (the vascular phase), helical CT can be used as a minimally invasive modality for vascular imaging that serves as an alternative to conventional angiography (7,9,11–16). Image postprocessing including multiplanar two-dimensional and three-dimensional reconstruction techniques on an independent workstation can then be used to directly image the proximal renal arteries and allows assessment of primary vascular disease (8,11,17). In most cases, threshold-based shaded-surface display or maximum-intensity projection images are generated from the data set of the original axial images for the three-dimensional presentation. In recent years, true volume-rendering techniques have taken full advantage of the volume data set and combined the advantages of both methods (16,18). A volume-rendered image on a workstation can be viewed in an interactive fashion, and overlying anatomic structures can be removed or highlighted for optimal morphologic demonstration (18). A cine review of axial source images on a workstation is useful for demonstrating small vessels and following their course (8).
Helical CT continues to evolve with the introduction of the new generation of CT scanners. With the introduction of a subsecond helical scanner and the more recent introduction of a multi–detector array scanner, a larger distance can be covered with similar collimation and pitch, or narrower collimation can be used while the same or a larger volume of data is acquired. Faster scanning techniques can optimize the timing of renal imaging during one particular phase of enhancement. In addition, section thickness can be retrospectively changed when multi–detector array techniques are used.
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Renal Trauma
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CT is highly accurate in evaluation of patients with suspected renal injuries after blunt trauma (19,20). In penetrating flank and back injuries, contrast-enhanced CT can be used to assess the extent of injury and potentially avoid surgical exploration (21). Blunt renal injuries are classified into four large categories: (a) minor injuries (renal contusion, intrarenal or subcapsular hematoma), minor lacerations with limited perinephric hematomas without extension to the medulla or collecting system, and small cortical infarcts; (b) major lacerations through the cortex extending to the medulla or collecting system with or without extravasation of urine; (c) catastrophic renal injuries including multiple renal lacerations, shattered kidney, and vascular injuries involving the renal pedicle; and (d) injuries of the UPJ (19,22). The presence of active bleeding is indicative of the third category of renal injuries (23). In selected patients in stable condition with active bleeding, intraarterial embolization can be the treatment of choice to maximize salvage of the renal parenchyma, although surgery may be required in patients in unstable condition with multiple injuries (23).
Primary vascular injury of the kidney following blunt trauma occurs when there is occlusion of the main renal artery by an intimal flap as a result of deceleration. Occlusion of a segmental renal artery branch results in a segmental renal infarct. On occasion, the diagnosis may be delayed because hematuria is absent. Renal pedicle injury is rarely associated with thrombosis or laceration of the renal vein (23,24).
CT Findings
In cases of posttraumatic occlusion of the main renal artery, contrast-enhanced helical CT is useful for detection of abrupt termination of the renal artery just beyond its origin (Fig 1) (25). In most cases, conventional angiography is not necessary to confirm the CT diagnosis.
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Figure 1. Global renal infarct in a 24-year-old man after blunt abdominal trauma. Contrast-enhanced helical CT scan shows abrupt termination of the proximal right main renal artery (solid arrow) without a nephrogram, findings consistent with renal artery occlusion. Note the retroperitoneal hematoma around the inferior vena cava (IVC) (open arrow).
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Typical parenchymal findings in posttraumatic occlusion of the main renal artery include an absent nephrogram with or without the cortical rim sign. A cortical rim of increased enhancement usually appears several days after injury (26) but has been reported to occur as early as 8 hours after injury (27). Segmental infarcts often appear as sharply demarcated, wedge-shaped areas of absent enhancement according to the distribution of the occluded vessel (Fig 2).
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Figure 2. Segmental renal infarct in a 34-year-old man after blunt abdominal trauma. Contrast-enhanced helical CT scan shows a sharply demarcated area of decreased enhancement in the posterior upper pole of the right kidney, a finding consistent with occlusion of the dorsal branch of the renal artery. Note the splenic laceration with a perisplenic hematoma (arrow).
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Absence of perinephric hematoma is a hallmark of renal artery occlusion unless associated renal lacerations are present. Hemorrhagic infiltration or minimal hematoma is present around the proximal renal artery.
Therapy
At presentation, most patients with traumatic renal artery thrombosis have irreversible ischemia of the kidney. In a review of the literature (28), among 35 patients with unilateral posttraumatic occlusion of a renal artery who underwent revascularization, only five (14%) had return of normal renal function; all five patients had an ischemic time of less than 12 hours. However, revascularization should be attempted when the patient has a solitary kidney or bilateral renal artery thromboses.
Posttraumatic Renovascular Hypertension
Posttraumatic renovascular hypertension is an uncommon complication of renal injury, although the precise prevalence is difficult to establish. In a recent review of seven cases of renovascular hypertension 2 weeks to 8 months after major blunt abdominal trauma, selective renal arteriography showed occlusion of the main renal artery in two patients, significant stenosis by an intimal flap in one patient, severe renal contusion in two patients, and segmental renal artery branch injuries in two patients (29). Rarely, chronic contained subcapsular hematoma or perirenal scarring creates a compressive force on the deformed kidney, reducing flow to the kidney and inducing renin-mediated hypertension (Page kidney). An arteriovenous fistula caused by deep renal laceration can result in renin-mediated hypertension by producing ischemia distal to the fistula.
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Arteriovenous Communications
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Arteriovenous communications can be congenital or acquired. They are direct communications from an artery to a vein without an intervening capillary bed.
Arteriovenous malformations (AVMs) are usually asymptomatic and are found more often in women than in men. Cirsoid AVMs consist of multiple small arteriovenous communications that are supplied by multiple segmental or interlobar arterial branches of normal caliber and tend to be located adjacent to the collecting system. Patients with AVMs often present with gross hematuria. An AVM is a rare cause of subcapsular or perinephric hematoma.
Arteriovenous fistulas comprise 70%–80% of arteriovenous communications in the kidney (30). Arteriovenous fistulas can result from trauma, surgery, tumors, inflammation, or erosion of an aneurysm directly into a vein (idiopathic arteriovenous fistula). Arteriovenous fistulas typically have a single feeding artery and a single draining vein, both of which are markedly enlarged. Arteriovenous fistulas are seen more often in men than in women because penetrating trauma is the most common cause. Although the prevalence of arteriovenous fistulas after trauma (eg, stab wound, percutaneous needle biopsy, percutaneous nephrostomy, nephrolithotripsy) is unknown, most are asymptomatic and close spontaneously within a few months. The most common clinical manifestation of a renal arteriovenous fistula is an abnormal bruit. Cardiomegaly or congestive heart failure occurs in one-half of symptomatic patients (30). Persistent or delayed hematuria is also common. Ischemia in the renal parenchyma distal to the arteriovenous fistula may induce renin-mediated hypertension and impaired renal function.
CT Findings
The CT appearance of arteriovenous communications depends on the timing of image acquisition relative to intravenous contrast material administration, the amount of contrast material, and the injection rate (31). Contrast-enhanced helical CT performed during the vascular and early cortical nephrographic phases is valuable in detection of an intrarenal vascular mass with feeding and draining vessels, which are usually engorged. There is prompt filling of the draining veins as well as the renal vein and IVC immediately after enhancement of the arteries (Fig 3) (30,32).
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Figure 3. Arteriovenous fistula in a 25-year-old man with a history of needle biopsy of the left kidney. Contrast-enhanced helical CT scan obtained during the early nephrographic phase shows marked enhancement in a large vascular lesion (V) and the left renal vein (straight arrow); the enhancement is similar to that in the aorta but greater than that in the right renal vein (curved arrow). The left kidney demonstrates a diminished nephrogram and atrophy (arrowheads), which are indicative of diffuse ischemia distal to the arteriovenous fistula.
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A diminished nephrogram with or without cortical atrophy distal to an arteriovenous fistula may be seen at helical CT; this appearance is most likely due to the decreased flow to the renal segment because of the shunt. When an AVM bleeds, an intraparenchymal hematoma is present. A subcapsular or perinephric hematoma may be present as a result of bleeding from an AVM.
Therapy
Conventional angiography may still be necessary for diagnosis and management (30,33). Transcatheter intraarterial occlusion, surgery, or a combination of these techniques is indicated in patients with symptoms including hypertension, congestive heart failure, and hematuria (30).
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Renal Artery Aneurysm
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The most common cause of aneurysms of the renal artery is atherosclerosis (34). Less common causes include medial fibroplasia, pregnancy, and mesenchymal diseases such as neurofibromatosis and Ehlers-Danlos syndrome. Renal pseudoaneurysms are usually posttraumatic or inflammatory (eg, Behçet's disease, mycotic aneurysm) (35,36). The prevalence of renal artery aneurysms is reported to be 0.01%–0.1% (37). Renal artery aneurysms account for 22% of visceral aneurysms (38). The prevalence of renal artery aneurysms at visceral conventional angiography ranges from 0.3% to 2.5%, depending on how patients are selected for investigation (38). Most patients are asymptomatic, and the aneurysm is often discovered incidentally during imaging or at autopsy (38). Renal artery aneurysms often contain mural thrombus and may give rise to emboli of the kidney. The risk of rupture is small, particularly when rimlike calcification is present in the wall of the aneurysm (38). The possibility of a ruptured renal artery aneurysm should be considered in pregnant women who present with evidence of retroperitoneal hemorrhage (38,39). Although hypertension is present in 70% of patients with renal artery aneurysm, a causal relationship has not been well documented (40).
Renal artery aneurysms can be classified into four types: saccular, fusiform, dissecting, and
intrarenal (41). Saccular aneurysms are usually present in the main renal branch near the first bifurcation and are associated with medial fibroplasia and atherosclerosis. Fusiform aneurysms are usually found in medial fibroplasia and are not calcified. Dissecting aneurysms, which may involve the main renal artery with or without extension to the segmental branches, may be classified according to cause as traumatic, spontaneous (eg, atherosclerosis, intimal fibroplasia, perimedial fibroplasia), and iatrogenic (eg, catheterization). Intrarenal aneurysms are frequently associated with arteritis (eg, polyarteritis nodosa, Wegener granulomatosis) but can also be caused by atherosclerosis, fibroplasia, trauma, vascular malformations, syphilis, tuberculosis, or tumors.
CT Findings
Most aneurysms are extrarenal. If calcified, a renal artery aneurysm can be recognized on plain abdominal radiographs. At CT, calcification is readily evident along the wall of the aneurysm and typically appears as an incomplete or complete ring of calcification (Fig 4) (42) or as a series of rings. After administration of contrast material, variable enhancement occurs, depending on the amount of mural thrombus within the aneurysm. Classically, arteriography is used for surgical planning. Helical CT angiography with two-dimensional and three-dimensional display can play a primary or complementary role in demonstrating the origin of the aneurysm and its relationship to the renal arteries (Fig 5). Contrast-enhanced helical CT performed with thin sections can show an intimal flap in the main renal artery, a finding consistent with dissection.
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Figure 4. Calcified renal artery aneurysm in a 60-year-old woman. Intravenous urography showed a ring of calcification in the proximity of the collecting system in the upper right kidney. Nonenhanced helical CT scan shows a calcified aneurysm (arrow).
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Figure 5a. Renal artery aneurysm in a 48-year-old woman. Intravenous urography showed extrinsic compression of the right renal pelvis superomedially. (a) Contrast-enhanced helical CT scan shows a well-defined round mass (A) in the renal hilum with enhancement similar to that of the vessel, findings consistent with an aneurysm. Selective digital subtraction angiography showed a large aneurysm in the region of the renal artery bifurcation. The location of the neck of the aneurysm was not clear at angiography. (b) Helical CT scan obtained during intraarterial injection of contrast material into the right main renal artery via a catheter shows an aneurysm (A) arising at the bifurcation of the main renal artery (mra) into the anterior segmental renal artery (asra) and posterior segmental renal artery (psra). The posterior segmental artery arises directly from the wall of the aneurysm. P = renal pelvis. (c) Color-encoded shaded-surface display image from the helical CT data clearly shows the relationship of the saccular aneurysm (A) to the main renal artery (mra), anterior segmental renal artery (asra), and posterior segmental renal artery (psra). The arteries and aneurysm are encoded red; the collecting system (P) is encoded yellow. The patient underwent resection of the aneurysm and autotransplantation of the kidney into the right iliac fossa.
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Figure 5b. Renal artery aneurysm in a 48-year-old woman. Intravenous urography showed extrinsic compression of the right renal pelvis superomedially. (a) Contrast-enhanced helical CT scan shows a well-defined round mass (A) in the renal hilum with enhancement similar to that of the vessel, findings consistent with an aneurysm. Selective digital subtraction angiography showed a large aneurysm in the region of the renal artery bifurcation. The location of the neck of the aneurysm was not clear at angiography. (b) Helical CT scan obtained during intraarterial injection of contrast material into the right main renal artery via a catheter shows an aneurysm (A) arising at the bifurcation of the main renal artery (mra) into the anterior segmental renal artery (asra) and posterior segmental renal artery (psra). The posterior segmental artery arises directly from the wall of the aneurysm. P = renal pelvis. (c) Color-encoded shaded-surface display image from the helical CT data clearly shows the relationship of the saccular aneurysm (A) to the main renal artery (mra), anterior segmental renal artery (asra), and posterior segmental renal artery (psra). The arteries and aneurysm are encoded red; the collecting system (P) is encoded yellow. The patient underwent resection of the aneurysm and autotransplantation of the kidney into the right iliac fossa.
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Figure 5c. Renal artery aneurysm in a 48-year-old woman. Intravenous urography showed extrinsic compression of the right renal pelvis superomedially. (a) Contrast-enhanced helical CT scan shows a well-defined round mass (A) in the renal hilum with enhancement similar to that of the vessel, findings consistent with an aneurysm. Selective digital subtraction angiography showed a large aneurysm in the region of the renal artery bifurcation. The location of the neck of the aneurysm was not clear at angiography. (b) Helical CT scan obtained during intraarterial injection of contrast material into the right main renal artery via a catheter shows an aneurysm (A) arising at the bifurcation of the main renal artery (mra) into the anterior segmental renal artery (asra) and posterior segmental renal artery (psra). The posterior segmental artery arises directly from the wall of the aneurysm. P = renal pelvis. (c) Color-encoded shaded-surface display image from the helical CT data clearly shows the relationship of the saccular aneurysm (A) to the main renal artery (mra), anterior segmental renal artery (asra), and posterior segmental renal artery (psra). The arteries and aneurysm are encoded red; the collecting system (P) is encoded yellow. The patient underwent resection of the aneurysm and autotransplantation of the kidney into the right iliac fossa.
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Nephrographic and perinephric abnormalities are absent in most cases. Perinephric hematoma may result from rupture of the aneurysm. Renal infarcts secondary to emboli from mural thrombus in the aneurysm may be seen at contrast-enhanced CT.
Therapy
A small (<2 cm in diameter), well-calcified renal artery aneurysm in a nonhypertensive, asymptomatic patient is treated conservatively (41). Surgical repair may be required when imaging studies show interval growth of an aneurysm and mural thrombus causing peripheral embolization or when an aneurysm occurs in a woman of childbearing age (41). Surgical intervention may also be indicated when an aneurysm is associated with diminished renal function, ischemia, hypertension, or dissection.
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Vasculitis
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Characteristic CT findings can be found in some of the diseases associated with vasculitis, although it is often difficult to distinguish between the various causative conditions with radiologic studies.
Polyarteritis Nodosa
Renal involvement occurs in 90% of patients with polyarteritis nodosa (43). Patients with polyarteritis nodosa often present with hematuria. Renal ischemia occurs as a result of involvement of medium-sized vessels, and renin-mediated hypertension is common.
CT Findings.—Occasionally, the "microaneurysms" in patients with polyarteritis nodosa may be seen at dynamic contrast-enhanced CT. Selective angiography typically shows small aneurysms at the bifurcation of the interlobar or arcuate arteries.
Contrast-enhanced CT can demonstrate areas of infarction of different ages. The kidneys may appear lobulated with irregular thinning of the parenchyma due to prior cortical infarcts (Fig 6) (44). The collecting system is usually preserved. Multiple linear bands of low attenuation may be present in the kidneys and are attributed to occlusion of intrarenal arteries.
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Figure 6a. Perinephric hemorrhage in a 40-year-old man with polyarteritis nodosa who presented with left flank pain of acute onset. Nonenhanced (a) and contrast-enhanced (b) helical CT scans show left perinephric (pn) and anterior pararenal (ap) hematomas, with a focal defect in the left renal cortex (arrow) shown on the contrast-enhanced scan (b). Note the multiple small focal areas of renal parenchymal scarring with a lobulated renal contour bilaterally. Selective right renal angiography showed small aneurysms.
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Figure 6b. Perinephric hemorrhage in a 40-year-old man with polyarteritis nodosa who presented with left flank pain of acute onset. Nonenhanced (a) and contrast-enhanced (b) helical CT scans show left perinephric (pn) and anterior pararenal (ap) hematomas, with a focal defect in the left renal cortex (arrow) shown on the contrast-enhanced scan (b). Note the multiple small focal areas of renal parenchymal scarring with a lobulated renal contour bilaterally. Selective right renal angiography showed small aneurysms.
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The small aneurysms in polyarteritis nodosa occasionally rupture and produce intrarenal, subcapsular, or perinephric hematoma (Fig 6).
Therapy.—Patients with polyarteritis nodosa are treated medically. In patients with perinephric hemorrhage who are hemodynamically unstable, selective angiography may be indicated to look for active bleeding; transcatheter embolization can then be performed, and surgery may be avoided.
Systemic Lupus Erythematosus
Renal disease occurs in 30%–50% of patients with systemic lupus erythematosus (SLE) and encompasses the entire spectrum of glomerular, tubular, or vascular disease (45). Many patients with SLE die of renal failure.
Patients with SLE have a high risk of developing a thrombus in the renal vein (45,46). One of the common causes of renal disease in SLE is membranoproliferative glomerulonephritis. One-third of SLE patients with nephrotic syndrome develop renal vein thrombosis. Therefore, renal biopsy is usually indicated. Thrombosis of the renal vein and IVC also occurs in SLE patients with thrombophlebitis.
CT Findings.—The larger lobular arteries are usually unaffected, but interlobular arteries may be affected by inflammatory changes and may be narrowed. Microaneurysms similar to those seen in polyarteritis nodosa are less frequently seen. Renal vein thrombosis is seen as a filling defect in a thick-walled renal vein with or without extension into the IVC on contrast-enhanced CT scans (45–47). Collateral vessels may be present along the proximal to middle ureter and at the renal hilum.
The kidney may be enlarged or diminutive depending on the stage of lupus nephritis. Multiple linear bands of a decreased nephrogram may be present as a result of associated vasculitis (Fig 7). In the acute or subacute phase of renal vein thrombosis, the affected kidney is enlarged and associated with coarse striations of a diminished nephrogram.
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Figure 7. Nephromegaly in a 21-year-old woman with SLE who presented with abdominal pain. Contrast-enhanced helical CT scan shows nephromegaly with peripheral hypoattenuating striations (arrowheads). Selective renal angiography showed peripheral defects in the nephrogram.
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Perinephric hematoma is rare in SLE. With renal vein thrombosis, soft-tissue stranding and collateral vessels are often present in the perinephric space.
Therapy.—Patients with SLE are treated medically. If the diagnosis of renal vein thrombosis is made, the treatment regimen includes anticoagulants to prevent pulmonary emboli.
Drug-induced Vasculitis
Vasculitis associated with intravenous drug abuse has clinical and pathologic features similar to those of polyarteritis nodosa (48). Although methamphetamine is a common drug used by patients in whom vasculitis develops, most patients are usually exposed to multiple drugs in addition. A variety of vascular problems associated with cocaine abuse have been reported, including neurovascular complications, cardiovascular complications, aortic dissection, venous thrombosis, mesenteric artery thrombosis, and renal infarction (49). Embolic infarction may occur when patients receive an injection of a foreign body secondary to impurities mixed with the drug, resulting in subacute bacterial endocarditis. CT may reveal renal infarcts of various size, number, and age (Fig 8).
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Figure 8. Drug-induced vasculitis in a 45-year-old man with a history of cocaine and other drug abuse. Contrast-enhanced helical CT scan shows multiple infarcts in both kidneys and the spleen (straight solid arrow). Note the thrombus secondary to vasculitis in the superior mesenteric artery (curved arrow) and aorta (open arrow).
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CT Findings.—Contrast-enhanced CT may show a mural thrombus or dissection in the visceral arteries. A mycotic aneurysm is occasionally seen. Renal infarcts caused by vasculitis or emboli appear as wedge-shaped areas of diminished excretion with or without a cortical rim of enhancement. Perinephric hematoma is an uncommon finding.
Therapy.—Patients are treated conservatively.
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Spontaneous Renal Hemorrhage
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Spontaneous (nontraumatic) renal hematoma may occur as a result of rupture of a renal tumor, vasculitis, hemorrhage from an aneurysm, hemorrhagic diathesis due to anticoagulant therapy or coagulopathy, infection, and acute or chronic nephritis (Table 1) (50). In a review of the literature through 1974, 33% of cases were due to renal cell carcinoma, 24% to angiomyolipoma, and 18% to vascular disease, with polyarteritis nodosa being the most common type (51). Patients with spontaneous perinephric hematoma typically present with flank pain of sudden onset. Hematuria is usually absent.
Patients being treated with systemic anticoagulant therapy may experience spontaneous hemorrhage. The prevalence of spontaneous hemorrhage among patients receiving intravenously administered heparin (4.3%–6.6%) is higher than that among patients receiving orally administered anticoagulants (0.1%–0.6%) (52,53). Hemorrhage as a complication of anticoagulant therapy can be found in the perinephric space, suburothelium or subepithelium (54,55), and renal sinus (56). The urinary tract may be a site of bleeding in up to 40% of patients receiving anticoagulants (57). Radiologic investigation and cystoscopy are warranted in patients receiving anticoagulants who experience gross hematuria (58). In a retrospective review of 24 patients who experienced gross hematuria while being treated with anticoagulants, intravenous urography and cystoscopy demonstrated the source of bleeding in 12 patients (50%); the source was a tumor in five patients, stone disease in four patients, hemorrhagic cystitis in two patients, and a calcified renal mass in one patient (58).
Renal Neoplasms That Cause Renal Hemorrhage
Twenty-five percent of cases of spontaneous renal hemorrhage are due to benign renal tumors, with angiomyolipoma being the most common type (50). Tuberous sclerosis is typically associated with bilateral renal angiomyolipomas. Sporadic angiomyolipomas are usually solitary. Among angiomyolipomas 4 cm or larger in diameter, 82%–94% are symptomatic and 50%–60% bleed spontaneously (59). Angiomyolipomas smaller than 4 cm in diameter are seldom symptomatic and less likely to bleed (60,61).
Renal cell carcinoma is also a cause of spontaneous renal hemorrhage. Because CT is highly sensitive in detection of renal cell carcinoma, absence of a renal mass virtually excludes this diagnosis. Renal cell carcinoma may be found in at least 50% of cases of spontaneous renal hemorrhage (52).
CT Findings
If the cause of a perinephric hematoma (eg, trauma, vasculitis, anticoagulant therapy, clotting disorder) is not apparent and initial CT does not show a cause, repeat tailored thin-section helical CT performed with and without intravenously administered contrast material is required to exclude a small renal cell carcinoma (43). Selective renal angiography may be necessary to exclude vascular lesions, including vasculitis, arteriovenous communications, and aneurysms, when a dedicated CT study does not demonstrate the source of the bleeding (50,53,62). If the cause of a perinephric hemorrhage remains indeterminate, follow-up CT at 3 and 6 months may be indicated.
Vascular manifestations are uncommon. The presence of fat within a renal mass at CT establishes the diagnosis of angiomyolipoma with near certainty (Fig 9). Renal cell carcinomas appear as rounded masses with heterogeneous attenuation (Fig 10). The diagnosis of renal cell carcinoma should be considered when an enhancing renal mass without appreciable fat is seen. Renal cell carcinomas may have dystrophic calcifications.
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Figure 9. Ruptured angiomyolipomas in a 32-year-old man with a history of tuberous sclerosis. Contrast-enhanced CT scan shows multiple large fat-containing masses involving the kidneys bilaterally. Note the large intratumoral hematoma (H) with a perinephric hematoma (arrow). The left kidney (LK) is displaced anteriorly.
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Figure 10. Ruptured renal cell carcinoma in a 60-year-old man. Contrast-enhanced CT scan shows a hypoattenuating mass (M) in the lower pole of the left kidney, which is displaced anteriorly by a perinephric hematoma with a fluid-fluid level (arrow). Selective renal angiography showed a hypovascular exophytic tumor in the lower pole of the left kidney with minimal coarse neovascularity.
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Various degrees of perinephric hematoma can be present (Figs 9 –11). Thickening of bridging septa in the perinephric space and thickening of the renal fascia are frequently present. A suburothelial hematoma appears as high-attenuation thickening of the wall of the renal pelvis and ureter (54,55). Hemorrhage into the renal sinus appears as a mass in the renal sinus with mass effect on the adjacent renal pelvis (Fig 12) (56). A blood clot in the renal pelvis may appear as a wall lesion, mimicking a renal pelvic mass.
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Figure 11. Perinephric hematoma in a 53-year-old woman receiving anticoagulant therapy. Contrast-enhanced CT scan shows areas of active bleeding (arrows) adjacent to the left kidney within a large perinephric hematoma of lower attenuation.
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Figure 12. Spontaneous renal sinus hemorrhage in a 72-year-old man receiving anticoagulant therapy. Contrast-enhanced CT scan shows a left renal sinus mass (H). Ureteroscopy showed no abnormality in the upper urinary tract. Note the thickening of the renal fascia (arrow).
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Therapy
Patients with small angiomyolipomas can be treated with observation. Intraarterial embolization may be indicated when tumors are larger than 4 cm in diameter and show signs of continued bleeding (59). Nephrectomy is performed in patients with renal cell carcinoma. Nephrectomy is also performed in patients with a normal contralateral kidney and persistent life-threatening hemorrhage, the source of which is not demonstrated at serial radiologic studies (53).
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Renal Infarct
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Renal infarction occurs in a variety of clinical settings (Table 2). The most common cause is thromboembolism from cardiovascular disease. The most common clinical manifestation is sudden onset of flank or back pain. Hematuria, proteinuria, fever, and leukocytosis may be present.
Although it is more common for venous thrombosis to be associated with malignancy (paraneoplastic syndrome), arterial thrombosis is also occasionally associated with malignancy (Fig 13); venous or arterial thrombosis may be the initial manifestation (63).
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Figure 13. Paraneoplastic thromboembolic disorder (Trousseau syndrome) in a 49-year-old woman with advanced pancreatic carcinoma. Contrast-enhanced helical CT scan shows a left renal infarct. Note the ill-defined, hypoattenuating mass (M) in the head of the pancreas with associated encasement of the superior mesenteric artery (open arrow) and thrombosis of the superior mesenteric vein (solid arrow). A filter is present in the IVC (C) for deep venous thrombosis. Two focal hypoattenuating metastases are present in the liver (arrowheads). Splenic and hepatic infarcts were also present.
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CT Findings
Vascular manifestations are uncommon. The parenchymal appearance depends on the size of the embolus, the location of the arterial occlusion, and its age. Contrast-enhanced CT readily demonstrates absence of enhancement in the affected renal tissue. Acute infarcts typically appear as wedge-shaped areas of decreased attenuation within an otherwise normal-appearing kidney. When large areas of the kidney are involved, an increase in the size of the kidney due to edema can be seen. In global infarction, the entire kidney is enlarged and its reniform configuration remains preserved. The cortical rim sign usually appears several days after onset of the infarction (Fig 14) (27). After the acute phase of renal infarction, atrophy begins. The infarcted tissue contracts, leaving a cortical scar (Fig 15). The extent and degree of parenchymal loss reflect the distribution of the affected artery and revascularization from collateral circulation. Perinephric manifestations are uncommon.
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Figure 14. Global renal infarct in a 21-year-old woman with polysplenia syndrome (polysplenia, situs ambiguous, and atrial septal defect) who presented with subacute bacterial endocarditis. Contrast-enhanced CT scan shows a global infarct of the right kidney with a rim of enhancement in the capsule (arrow). A = aorta, C = IVC, L = liver, S = spleen.
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Figure 15a. Renal infarct in a 46-year-old woman with a thrombus in the thoracic aorta who experienced multiple episodes of thromboembolism. (a) Contrast-enhanced CT scan shows a wedge-shaped area of decreased enhancement (arrow) in the left midkidney, a finding consistent with a focal infarct. (b) Follow-up contrast-enhanced CT scan obtained 6 months later shows a cortical scar (arrow). (c) Sagittal reformation image of the thorax shows an irregular filling defect (arrow) in the descending aorta. Thrombectomy of the descending aorta was performed.
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Figure 15b. Renal infarct in a 46-year-old woman with a thrombus in the thoracic aorta who experienced multiple episodes of thromboembolism. (a) Contrast-enhanced CT scan shows a wedge-shaped area of decreased enhancement (arrow) in the left midkidney, a finding consistent with a focal infarct. (b) Follow-up contrast-enhanced CT scan obtained 6 months later shows a cortical scar (arrow). (c) Sagittal reformation image of the thorax shows an irregular filling defect (arrow) in the descending aorta. Thrombectomy of the descending aorta was performed.
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Figure 15c. Renal infarct in a 46-year-old woman with a thrombus in the thoracic aorta who experienced multiple episodes of thromboembolism. (a) Contrast-enhanced CT scan shows a wedge-shaped area of decreased enhancement (arrow) in the left midkidney, a finding consistent with a focal infarct. (b) Follow-up contrast-enhanced CT scan obtained 6 months later shows a cortical scar (arrow). (c) Sagittal reformation image of the thorax shows an irregular filling defect (arrow) in the descending aorta. Thrombectomy of the descending aorta was performed.
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Therapy
Anticoagulant therapy is usually instituted. Thrombolytic therapy, transcatheter thromboembolectomy, supportive hemodialysis, or surgical treatment may be indicated in patients with bilateral renal emboli, an embolus to a solitary kidney, or unilateral complete renal embolic occlusion.
Acute Cortical Necrosis
Acute cortical necrosis, a rare form of acute renal failure, results from ischemic necrosis of the renal cortex with sparing of the renal medulla. The pathophysiology of this condition is complex and has been attributed to ischemia due to vasospasm of small vessels, toxic damage to glomerular capillary endothelium, and primary intravascular thrombosis (64). The process is either multifocal or diffuse; in most cases, it is bilateral. This condition is associated with complications of pregnancy, including abruptio placentae and septic abortion. Other causes include sepsis, shock, venomous snake bite, severe dehydration, transfusion reaction, and hemolytic uremic syndrome. Cortical necrosis can result from any condition that produces acute, prolonged shock.
The radiographic findings vary with the extent and stage of the disease. In the early phase, the kidneys are diffusely enlarged and poorly visualized.
Helical CT performed during the arterial phase can show enhancing interlobar and arcuate arteries adjacent to the nonenhancing cortex (65). Characteristic parenchymal findings include enhancement of the medulla but no enhancement of the cortex (Fig 16) (66–68). A rim of subcapsular cortical enhancement is also a characteristic finding because of collateral flow from the capsular vessels (Fig 17). Enhancement of the juxtamedullary zone of the cortex may be present. Therefore, the necrotic cortex appears as a hypoattenuating zone circumscribing the kidneys adjacent to the renal capsule. Renal function is usually diminished. The kidneys become progressively smaller over several months. A single thin rim of calcification or "tramline" calcification can form in the renal cortex (42). The characteristic cortical calcification appears as early as 1–2 months after the event. There are no perinephric manifestations.
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Figure 16a. Acute cortical necrosis in a 65-year-old woman who underwent bowel resection for an incarcerated ventral hernia. (a) Preoperative contrast-enhanced CT scan shows normally functioning kidneys. The postoperative course was complicated by sepsis. (b) Follow-up contrast-enhanced CT scan obtained 7 days after surgery shows bilateral lack of enhancement of the renal cortex.
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Figure 16b. Acute cortical necrosis in a 65-year-old woman who underwent bowel resection for an incarcerated ventral hernia. (a) Preoperative contrast-enhanced CT scan shows normally functioning kidneys. The postoperative course was complicated by sepsis. (b) Follow-up contrast-enhanced CT scan obtained 7 days after surgery shows bilateral lack of enhancement of the renal cortex.
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Figure 17. Acute cortical necrosis in a 13-year-old girl with sepsis. Contrast-enhanced helical CT scan shows lack of enhancement of the renal cortex. Note the narrow subcapsular rim of enhancement (arrows).
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Renal Artery Stenosis
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Renovascular hypertension accounts for 1%–4% of all patients with hypertension (69). Renovascular hypertension is renin-mediated and occurs as a response to renal ischemia. Atherosclerosis accounts for approximately two-thirds of patients with significant narrowing of the main 
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Abstract
LEARNING OBJECTIVES FOR TEST...
