Solitary filling defects of the ureter

Solitary

Filling

Defects of the Ureter

By Alan B. Fein and Bruce L. McClennan

M

ANY NORMAL and abnormal conditions produce a solitary filling defect in the contrast-filled ureter (Table 1). We present a systematic approach by which these defects can be detected and defined using a variety of imaging techniques.

opacified urine. A soft tissue lesion may be present in the ureter and not appreciated by CT due to failure to image the involved segment of the ureter or to lack of sufficient resolution, and contrast to differentiate a small soft tissue mass from a normal collapsed ureter. An artifactual lesion may be produced by volume averaging, ureteral peristalsis, or patient motion.3.4 A recent addition to the armamentarium of techniques capable of imaging the ureter and renal pelvis is magnetic resonance imaging (MRI). Although no definite role has yet been established for MRI of the ureter, the capability of multiplanar imaging and the possible use of gadolinium as a contrast agent may prove effective in demonstrating ureteral involvement from an adjacent retroperitoneal inflammatory or neoplastic process. Although ultrasound, radionuclide scanning, and angiography may be potentially useful in demonstrating the size, course, and patency of the ureter, they seldom have utility for detecting and evaluating a solitary filling defect.

RADIOLOGIC DETECTION

The initial diagnosis of ureteral pathology invariably relies upon a radiologic examination. This process should begin with a plain radiograph of the abdomen. Although the ureter itself is not visible, valuable information relating to the nature of the ureteral pathology may be present, such as a radiopaque calculus, calcium-containing neoplasm, or foreign body. On intravenous urography, opacification of the ureters normally begins at approximately 3 minutes, with maximum contrast density and ureteral filling occurring five to ten minutes after injection. The urographic examination should include at least AP, right and left posterior oblique, and postvoiding views that include the full extent of the ureters while they are maximally opacified. If portions of the ureter are not adequately visualized, ureteral compression may be used to achieve maximal filling, especially of the proximal two-thirds. Prone films may demonstrate the more anteriorly positioned midportion of the ureter to best advantage. Delayed films may occasionally be helpful. Failure to satisfactorily opacify the ureters by intravenous urography and clinical suspicion of intraluminal pathology are indications for retrograde ureteropyelography. Scout films, AP and oblique views after contrast medium injection, postdrainage films, and fluoroscopy (in selected cases) are of value in such cases. Antegrade ureteropyelography using percutaneous access may be indicated. In some cases, the distal and even the proximal ureters may be well visualized at cystography if there is vesicoureteral reflux.1*2 CT may be useful in identifying a soft tissue mass or a calculus within the ureter. The extraluminal extent of a lesion may be determined by CT scanning, but the exam should first be performed without intravenous contrast medium to avoid obscuration of the lesion by contrast Seminars in F?oantgeno/ogy,

Vol XXI, No 3 (July), 1986: pp 201-2

ARTIFACTS AND NORMAL VARIANTS

When confronted with an apparent ureteral filling defect, one must ask two basic questions prior to embarking on a long list of differential diagnostic possibilities: Could this be an artifact? Could this be a normal variant? The most common anatomic artifacts that simulate a ureteral filling defect are an overlying intestinal gas bubble or ureteral peristalsis producing an apparent lucency or unfilled segment in the contrast-filled ureter. Such a defect is

From the Mallinckrodt Institute of Radiology, Washington University School of Medicine, St Louis. Alan B. Fein: Instructor in Radiology, Mallinckrodt Institute of Radiology, Washington University School of Medicine; Bruce L. McClennan: Professor of Radiology, Mallinckrodt Institute of Radiology, Washington University School of Medicine. Address reprint requests to Bruce L. McClennan. MD, Mallinckrodt Institute of Radiology, Washington University School of Medicine, 510 South Kingshighway Blvd. St Louis, MO 631 IO. 0 1986 by Grune & Stratton, Inc. 0037-l 98X/86/21 02-0005$05.00/0

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Table

1. Causes

of Solitary

Ureteral

McCLENNAN

Filling Defect

Common stone Neoplasm, eg, transitional cell carcinoma Blood clot Vascular imprint Kinks Uncommon or Rare Sloughed papilla Fungus ball Metastasis Neoplasm, squamous cell carcinoma, adenocarcinoma, or nonepithelial Leukoplakia/cholesteatoma Malakoplakia Fibroepithelial polyp Nonspecific granuloma Amyloidosis Endometriosis Congenital web Cyst, congenital

usually transient and can be easily differentiated from an organic lesion with oblique views and sequential filming. A technical artifact due to a defect in the intensifying screen or to film processing is usually discovered by its inconstant appearance on sequential films. Normal Vascular Impressions Normal vessels may produce a persistent compression defect on the ureter that can be mistaken for intrinsic pathology. These include accessory renal artery or vein, an iliac vessel, and gonadal vessel. Generally a vascular impression can be identified by its location and linear imprint. Occasionally angiography may be necessary to confirm the vascular etiology of a ureteral filling defect.’ An accessory renal artery or vein is present in approximately 20% to 30% of the population. It may arise from the main renal artery or vein or directly from the aorta or inferior vena cava, respectively. The iliac vessels frequently produce a vascular impression on the ureter as it crosses the pelvic brim. This is explained by the relatively fixed position of the ureter at this location, which facilitates compression by adjacent structures. The gonadal vessels normally lie lateral or anterolateral to the ureter and may imprint the ureters as they course medially at the level of the L3 or L4 vertebral bodies. It is common to see an oblique indentation of the ureter at this level (Fig l), particularly in multiparous women.6

Fig 1. Gonadal artery imprint. (A) Oblique film from intravenous urogram demonstrates a smooth linear filling defect in the proximal ureter (arrow). (B) Selective renal artery injection reveals the gonadal artery (arrow) imprinting the ureter, producing the defect.

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Although it is well known that vascular collaterals secondary to renal artery stenosis, aortic or iliac artery occlusion, arteriovenous fistula, shunting through a renal neoplasm, inferior vena cava or azygos vein occlusion, or portal hypertension may produce ureteral filling defects, these are almost invariably multiple and are discussed elsewhere in this issue. CONGENITAL

ABNORMALITIES

Transverse Folds

Single or multiple linear radiolucencies may be identified in the proximal ureter of infants with an otherwise normal urinary tract. This finding corresponds to the presence of one or more thin transverse folds composed of a full thickness inward projection of the ureteral wall. The fold is thought to represent persistent normal fetal tortuosity of the ureter, and usually resolves with further growth and development.7 It should not be confused with a transient kink or ureteral spasm. Ureteral Folds And Kinks

In some patients, a prominent psoas muscle will produce a transverse fold at the junction of the upper and middle thirds of the ureter which may be mistaken for a filling defect. This fold typically has a linear configuration that will vary over time and with changes in patient position. Occasionally an acquired kink in the ureter will produce a filling defect. This typically occurs at a point where the ureter bends to conform to the surrounding bony anatomy, such as the sciatic notch. A ureteral kink may also result from adhesionscaused by a persistent congenital connective tissue band or by previous surgery.8 Although a ureteral kink (Fig 2) usually has no clinical or physiologic significance, it may lead to obstruction if associated with other abnormalities, such as herniation of abdominal or pelvic contents through the inguinal, femoral, or sciatic foramen.’ Longitudinal striations of the proximal ureter rarely produce a ureteral filling defect. These may be normal but are usually seenin the setting of chronic mucosal inflammation or high volume states. Most often the striations are multiple, but occasionally a single fold may occur and be difficult to differentiate from a structural abnor-

Ureteral kink simulating Fig 2. AP view demonstrates an apparent ureter (arrow). (B) Oblique view. head) accounts for the opacity.

a ureteral calculus. (Al opacity in the proximal A ureteral kink (arrow-

mality. The longitudinal direction, smooth and delicate nature of the filling defect, and its disappearance when the ureter is distended are usually sufficient to indicate the true nature of this finding.” Congenital Valves and Webs

Valve-like folds of redundant mucosa may be present in the fetal ureter, the majority located in the inferior ureteral segment. These folds normally disappear with maturation but may persist, producing solitary or multiple ureteral filling defects and a varying degree of obstruction.”

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Congenital Ureteric Cysts Several cases of congenital cyst of the ureter have been reported. These may be associated with other abnormalities of ureteral development or may be seen in an otherwise normal ureter. The filling defect resulting from a urotheliumlined cyst may be confused with that of an ectopic ureterocele when it occurs at the ureterovesical junction (UVJ). It may simulate a ureteral tumor if it produces an isolated filling defect in other ureteral segments (Fig 3). The fluid-containing cyst is typically lined with urothelium and fibrovascular tissue.‘* INFLAMMATORY

LESIONS

LeukopIakia/Cholesteatoma Leukoplakia and cholesteatoma are manifestations of squamous metaplasia of the transitional epithelium with associated keratinization and desquamation. Rarely, the desquamated keratin accumulates rapidly, forming a focal mass termed a cholesteatoma. Although the etiology is uncertain, most authors feel that leukoplakia is secondary to chronic inflammation. However, occasional cases have been reported in the absence of any evidence of an inflammatory process. It is generally accepted

(B) CT scan reveals a low attenuation Fig 3 (can’t). nonenhancing lesion surrounded by contrast medium (arrowheads). It?.) Ultrasound scan demonstrates a sonolucent area with good through transmission [arrowheads) corresponding to the lesion. Pathologically proven. K = kidney: L = liver.

Suburothelial cyst. (A) IVU in AP view demonFig 3. strates a large, smooth, round filling defect in the renal pelvis and proximal ureter (arrow).

that leukoplakia implies an increased potential for malignant neoplasm in the affected kidney and ureter. Radiographically, leukoplakia is usually manifested on intravenous urography by solitary or multiple irregular filling defects in the proximal ureter or renal pelvis. Cholesteatoma presents as a solitary intraluminal filling defect or nodularity that may calcify or coalesce to form a discrete mass, and may be associated with obstruction. The diagnosis of leukoplakia or cholesteatoma can be established by brush biopsy.‘3-‘5 Malakoplakia refers to umbilicated yellowish

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plaques that correspond histologically to submucosal collections of phagocytic mononuclear cells with vacuolated eosinophilic cytoplasm and Michaelis-Gutmann bodies. It is thought to be related to infection and usually occurs in the bladder, although it may rarely involve the ureter primarily. In contradistinction to leukoplakia, malakoplakia has no known premalignant potential. Radiographically, ureteral malakoplakia presents as single or multiple filling defects, sometimes associated with obstruction (Fig 4). 16,17 Nonspecific Granuloma Rarely, a solitary ureteral filling defect may be produced by infiltration of the muscularis layer with histiocytes. This condition has been termed nonspecific granuloma and may be visualized as a pedunculated or sessile tumor projecting into the lumen, an intramural nodule, or a diffuse thickening of the wall. The condition affects both sexes equally and may involve the ureter at any level, either unifocally or at multiple sites.‘8.‘9 Fungus Ball Another cause of a solitary ureteral filling defect is a fungus ball. This is a manifestation of fungal infection, usually occurring in a diabetic or other immunocompromised hosts. The most common etiology is Candida albicans infection, although other organisms, such as Aspergillus fumigatus, have also been reported. Mechanisms of spread include hematogenous seeding, direct extension from the renal parenchyma or adjacent organs, ascending or descending ureteral spread, ureterointestinal fistula, or spread via instrumentation. The pyelographic appearance is that of an irregular rounded ureteral filling defect that may be associated with obstruction. There may be ureteral irregularity if the fungus infection is associated with microabscess formation. CT may be useful in characterizing the location and extent of the lesion.*&** Schistosomiasis Urinary bilharziasis due to infection with Schistosoma hematobium has a high prevalence in several geographic areas, including the Middle East, Central Africa, and South Africa. Ureteral involvement, more common in males, may occur

Malakoplakia. (A) IVU. irregularly marginated Fig 4. filling defect (arrow) producing obstruction at the level of the renal pelvis. (B) Retrograde ureterogram with ureteral stent in place shows an irregular filling defect extending into the proximal ureter (arrows). Brush biopsy confirmed the diagnosis of malakoplakia.

as a result of direct spread from the bladder or by hematogenous seeding of ova in the ureteric veins and branches of the superior mesenteric veins. Approximately one third of cases demonstrate macroscopic ureteral involvement, usually involving both lower ureteral segments, but occasionally presenting as unilateral focal disease. Rarely urinary schistosomiasis may present radiographically as a solitary ureteral filling

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McCLENNAN

defect due to the reaction incited by deposition of ova in the submucosal layer of the ureter. This may lead to fibrosis and calcification in the involved segment. Stricture, stenosis, or focal granulomas may result, producing a lesion that projects into the lumen and may be associated with obstruction. When calcified, lesions may be difficult to differentiate from ureteral cal-

Papillary

Necrosis

Necrosis of renal papillae may be seen in the setting of analgesic abuse, diabetes mellitus and other microvascular diseases, urinary tract infections, renal vein thrombosis, prolonged hypotension from any cause, urinary tract obstruction, sickle cell disease, nonsteroidal anti-inflammatory drug ingestion, and factor VIII or IX deficiency. The sloughed portion of the papillary tip may lodge in the renal pelvis or ureter, often producing a ureteral filling defect with obstruction. The obstructing papilla is radiographically nonopaque but may contain a ring-like calcification. A papilla lodged in the ureter usually passes spontaneously and can be identified histologically when recovered from the urine (Fig 5).25 PRIMARY NEOPLASMS

Primary neoplasms of the ureter are those which arise from its component structures. Ureteral neoplasms comprise approximately 1% of all cancers of the upper genitourinary tract. They are characterized as epithelial or mesodermal. The epithelial neoplasms are virtually all malignant or have malignant potential, while the mesodermal are almost always benign.26 In large series, about 75% of ureteral neoplasms are carcinomas, 2 1% are papillomas, and 4% are sarcomas, hemangiomas, or fibrous neoplasms.*’ Ureteral neoplasms have a 2:l male predominance, most cases presenting from the fourth to the seventh decade. They are most commonly located in the inferior third of the ureter, slightly more often on the right. Benign neoplasms, although less frequent, are twice as likely to be multiple. A number of primary malignant neoplasms of the ureter have been reported in childhood. They include benign polyps, spindle cell sarcoma, Wilms’ tumor, renal cell carcinoma, hamartoma,

Sloughed papilla. (A) A renal papilla has proFig 5. duced a well-defined filling defect in the distal right ureter (arrow). (6) Normal distal right ureter following catheter manipulation of papilla into urinary bladder. (Courtesy of Barry Katzen, MD, Alexandria, Va.)

reticulum cell sarcoma, transitional ma, and leiomyoma.28

cell papillo-

Malignant Nonepithelial Neoplasms These are extremely rare and include a variety of sarcomas, eg, reticulum cell sarcoma, leiomyosarcoma, and carcinosarcoma. Hodgkin’s disease

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and primary melanoma involving the ureter have also been reported.29 Malignant

Epithelial

Neoplasms

Malignant neoplasms of the ureter can be divided into epithelial and mesenchymal types. The vast majority are epithelial, the mesenchyma1 forms being exceedingly rare. Epithelial neoplasms may be classified by their histologic characteristics. The major categories are transitional cell carcinoma, squamous cell carcinoma, and primary mutinous adenocarcinema. Only 40% of papillary tumors are infiltrating at the time of diagnosis, as compared to nearly 100% of nonpapillary solid tumors, including transitional cell carcinoma and squamous cell carcinoma, which are the most malignant of the epithelial ureteral neoplasms (Fig 6). Epithelial neoplasm of the papillary type has a marked tendency to be multicentric, or associated with neoplasms elsewhere in the urinary tract; nonpapillary lesions are almost uniformly

solitary. Therefore, whenever a solitary ureteral filling defect due to an epithelial tumor is encountered, the entire urinary tract as well as the bladder must be evaluated to exclude the presence of synchronous lesions. When multiple lesions are present, they are usually ipsilateral and may be either synchronous or metachronous. Several cases have been reported in which bilateral ureteral tumors were present at the time of diagnosis; approximately 50% of these will demonstrate bladder involvement.3s33 Radiographically, a papillary tumor presents on urography as an isolated filling defect, often with irregular borders. Bergman et a134 have noted that in contrast to an obstructing calculus, a ureteral neoplasm will often result in dilatation of the ureter immediately below as well as above the tumor site. Often only the superior or inferior margin is outlined by contrast, the inferior contour having a meniscus type of appearance (Fig 7). Squamous cell carcinoma. The most malignant of the epithelial ureteral neoplasms, squamous cell carcinoma is almost always an infiltrating lesion of the nonpapillary type. It is often associated with chronic infection and urinary calculi. Urographically it most often appears as an irregularly marginated solitary lesion involving the full circumference of the ureter and associated with obstruction.35 Adenocarcinoma. Primary adenocarcinoma of the ureter is extremely rare, with less than 12 cases reported. It is often associated with urolithiasis and may present a confusing picture when associated with acute obstruction secondary to a calculus. Ureteral adenocarcinoma is more frequently metastatic, from an adjacent or distant primary neoplasm.36 Nonpapillary Tumors. The nonpapillary type of transitional cell carcinoma usually produces a small solitary lesion that appears on urography as a subtle intraluminal filling defect or as an area of eccentric focal narrowing that may be confused with a benign ureteral stricture.37 Metastasis

Fig 6. Invasive transitional cell carcinoma. Retrograde ureterogram shows an irregular “apple core” type of circumferential filling defect (arrowheads) involving the distal left ureter in a patient with microscopic hematuria. Proved at operation.

Metastatic disease may involve the ureter either by direct spread or by spread from a distant primary site. Direct extension may occur from retroperitoneal tumors such as lymphoma

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Fig 8. Metastatic disease. Retrograde ureterogram. A primary rectal carcinoma had been resected. The retrograde study demonstrates right ureteral obstruction and a well-defined intraluminal filling defect (arrow) proven to be metastatic colon carcinoma by biopsy.

Fig 7. Transitional cell carcinoma with Bergman’s sign. Retrograde ureterogram shows an irregularly marginated filling defect in the proximal left ureter with pyelocaliectasis above and ureteral dilatation immediately below the filling defect (arrow). suggesting a malignant tumor.

or pancreatic carcinoma. Obstruction of the ureter secondary to direct extension from cervical carcinoma is also common. Rarely colon carcinoma will involve the ureter via direct spread (Fig 8). A variety of primary tumors may seed the ureter with metastatic deposits. The most common primary sites are the renal parenchyma, stomach, prostate, breast, and 1ung.38*3g Recently a case of ureteral filling defect with obstruction considered secondary to myeloma protein deposition in multiple myeloma has been reported.40 Benign Neoplasms In this discussion all benign neoplasms will be considered nonepithelial in origin. The so-called

benign papilloma, an epithelial tumor with a low grade malignant potential, has been considered as a papillary transitional cell epithelioma, grade I (Broder’s classification) and has been discussed with the epithelial tumors. Benign tumors of the ureter are rare. They may be composed of any mesenchymal connective tissue element. In a large review, Bustos et a14* reported 78 cases, including fibroepithelial polyp, inflammatory polyp, fibroma, fibrolipoma, leiomyoma, granuloma, hamartoma, hemangioma, endometrioma, lymphangioma, myoma, and neurofibroma (Fig 9).4’

Fibroepithelial polyp. The most commonly detected benign ureteral tumor is the polyp, which histologically has a core of fibrous connective tissue covered by a layer of normal transitional cell epithelium. It is usually found in the proximal ureteral segment and is almost always solitary. Radiographically, the fibroepithelial polyp presents as a smooth, well-defined filling defect surrounded by a thin rim of contrast. It may be quite large and, when pedunculated, may be mobile, occupying different positions in the ureter over time with a variable degree of ure-

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DEFECTS

Fig 9. Schwannoma of the ureter. IVU shows a smooth crescentic filling defect (arrows) at the right UVJ with dilatation of the distal ureter. U = ureter; 6 = bladder.

teral obstruction. The stalk may be appreciated on some views (Fig lo), but this is inconsistent4* Nonpolypoid benign ureteral neoplasms typically present as a constant well-defined filling defect with smooth borders. Endometriosis. Endometriosis is defined as the presence of endometrial glandular tissue and stroma outside the uterine cavity. Involvement of the urinary tract is rare, occurring in 1% of patients with endometriosis. The bladder is affected most often. Over 100 cases of ureteral endometriosis have been reported. It usually affects women from 25 to 50 years of age, about 10% of whom are postmenopausal and 50% nulliparous. Endometrioisis of the ureter may be extrinsic or intrinsic. In the more common extrinsic form, endometrial glands and stroma are present in the adventitia or periureteral connective tissue, producing extrinsic compression and narrowing. In the intrinsic form, glands and stroma involve the lamina propria or muscularis of the ureter.43*44 Radiographically, the intrinsic form may produce solitary or multiple ureteral filling defects with or without obstruction, or a stricture that tends to be smooth with abrupt margins but without significant “shouldering.” Most cases involve the distal ureter, caudal to the pelvic brim. Possible mechanisms include direct invasion by endometrial tissue, transtubal seeding, lymphatic or hematogenous spread, implantation

Ureteral polyp. IVU shows a small rounded Fig 10. filling defect on a stalk Iarrows) found to be mobile on sequential films. Pathologic diagnosis: fibroepithelial polyp.

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secondary to surgery or trauma, metaplasia.45*46

and serosal

URETERAL CALCULUS

Ureteral calculus may be considered primary or secondary, depending on whether it originates in the ureter or merely occupies the ureter during passage from the kidney to the bladder. The secondary calculus may pass spontaneously, producing a transient solitary filling defect, or may become impacted in the ureter and result in a fixed filling defect with or without obstruction. The secondary calculus is the most frequently encountered cause of a solitary ureteral filling defect. The rare primary ureteral calculus occurs with ureteral stricture and infection, and in patients with schistosomiasis. Urinary calculi consist of approximately 98% crystalloids and 2% organic matrix. In the US, the major types of stone and their frequency are as follows: calcium oxalate, 73%; magnesium ammonium phosphate, 9%; calcium phosphate, 8%; uric acid, 7%; and cystine, 1%.47 Systemic illnesses that predispose to hypercalcemia and the formation of calcium-containing stones include hyperparathyroidism, hyperthyroidism, Cushing syndrome, milk-alkali syndrome, sarcoidosis, renal tubular acidosis, medullary sponge kidney, inflammatory bowel disease, multiple myeloma, metastatic disease to bone, and idiopathic hypercalciuria. Some less common metabolic disorders that may result in calculus formation include cystinuria, xanthinuria, and oxalosis. Patients with hyperuricemia and elevated urinary uric acid levels have a higher incidence of both calcium oxalate and uric acid stones.48 Urinary tract infection with urea-splitting organisms such as Proteus mirabilis and some forms of Klebsielfa tend to have an abnormally basic urine (pH greater than 7.5), which predisposes to formation of magnesium ammonium phosphate calculi, often termed struvite stones. These tend to be large, modestly radiopaque, laminated stones that may grow rapidly to fill the entire collecting system as a staghorn calculus. The incidence of urinary stone formation in the US is estimated at 0.1%. Calculi occur more frequently in men, with the exception of struvite stones, which have a high incidence in women owing to their higher rate of urinary infection

McCLENNAN

with urea-splitting organisms. The ureters are involved with equal frequency. Bilateral ureteral calculi are present in 2% to 4%. The three most frequent sites of impaction are the ureteropelvic junction, the level of the pelvic brim, and the ureterovesical junction (Fig 11). The radiographic appearance of a ureteral calculus depends upon its chemical composition, size, shape, and location within the ureter. On the plain film, the calcium oxalate stones are the most radiopaque; magnesium ammonium phosphate stones are of intermediate radiopacity; cystine stones are faintly radiopaque; uric acid stones are nearly radiolucent. It should be remembered that all stones are potentially opaque on CT if the area of interest is successfully localized for cross-sectional imaging. Furthermore, the high attenuation value of the calculus allows differentiation from truly radiolucent filling defects, such as blood clot or tumor.49 On plain films, the ureteral calculus may be difficult to differentiate from an overlying bowel opacity, bony structure, vascular wall calcification, phlebolith, lymph node calcification, or soft

Fig 11. Ureteral calculus. shows a calculus that has formed the distal left ureter (arrow).

Retrograde ureterogram around a surgical staple in

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Fig 12. Calculus in a simple ureterocele. The plain film had revealed a radiopaque stone in the expected position of the left ureterovesical junction. IVU shows the calculus as a radiolucent rim (solid black arrow) surrounding a central nidus within the contrast-filled, simple ureterocele (small arrows).

tissue calcification. The location and characteristics of the opacity as well as its position on oblique and tomographic films before and after contrast administration will generally serve to exclude these conditions. When a ureteral calculus is a clinical consideration, attention to certain aspects of the urogram becomes particularly important: (1) careful scrutiny of the scout film, including use of oblique views; (2) avoidance of compression, as this may make the presence and point of obstruction difficult to determine; (3) postcontrast oblique films, particularly important in determining if an opacity or lucency truly lies within the ureter; (4) columning of the contrast medium in the ureter with or without ureteral dilataton, which should be a “red flag” indicating the possibility of an obstructing lesion; (5) delay in appearance of contrast excretion and visualization of the kidney, with late films obtained to determine the level of obstruction; and (6) a postvoiding film, of particular benefit in establishing the presence and degree of obstruction, especially in cases when the distended bladder overlies the point of obstruction. A congenital abnormality such as a duplicated system may not be visualized initially, especially if it harbors an obstructing stone (Fig 12). Depending on the results of the intravenous urogram and the clinical status of the patient, plain films may be used to follow the progress of the ureteral calculus. CT or retrograde pyelography may be used to localize a nonopaque calculus. In our experience, a calculus of 5mm or less in

greatest diameter will almost always pass spontaneously with observation, hydration, and appropriate analgesia. Calculi measuring 5 to 8 mm will pass spontaneously in approximately 50% of patients. Calculi greater than 8 mm in maximal dimension rarely pass and require retrograde, percutaneous, or surgical manipulation. MISCELLANEOUS

Hemorrhage Intramural or intraluminal blood in the ureter may produce a solitary ureteral filling defect.

Fig 13. lntraluminal ureteral clot. IVU In a patient on systemic anticoagulants who developed hematuria. demonstrates an unusually shaped, oblong, irregular, lucent filling defect in the proximal ureter (arrow). It passed spontaneously during urogrephy.

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Intraluminal clot may result from instrumentation, blunt or penetrating injuries, any bleeding source within the kidney or ureter, or from spontaneous hemorrhage in a patient with a primary or secondary bleeding diathesis. The most common causes of intraluminal clot are chronic anticoagulation therapy and genitourinary instrumentation. Intraluminal clot presents as an irregular, often unusually shaped intraluminal filling defect that typically passes or resolves spontaneously due to the action of endogenous urinary urokinase. The time course of resolution is variable but usually occurs within a few days (Fig 13)?5 Primary Amyloidosis

of the Ureter

Primary amyloidosis is characterized by the deposition of hyaline glycoprotein substances around collagen fibers, most typically occurring in the heart, skeletal muscle, spleen, and blood vessels. Primary amyloidosis of the ureter is extremely rare, with less than 20 cases reported. The entire ureter may be involved or there may be localized involvement of the renal pelvis and upper third of the ureter, isolated involvement of the upper third of the ureter (one case), or isolated involvement of the distal third of the ureter (11 cases). Isolated involvement of the middle third of the ureter has not been reported. Urographic presentation is that of a filling defect or stricture with shelved margins and dilatation of the proximal and distal ureter which cannot be radiographically distinguished from neoplasm.52-55 REFERENCES 1. Pfister RC, Newhouse JH: Radiology of ureter. Urology 1978;12:15-39 2. Friedenberg RM, Bottizer WE: Radiographic examination of the ureter. In: Bergman H (ed): The Ureter (ed 2). New York: Springer-Verlag, 198 1;303-321 3. Ryan KG, Hoch WH, Craven RM: Intraureteral tumor demonstrated by computed tomography. J Comput Assist Tomogr 1979;3:474477 4. Federle MP, McAninch JW, Kaiser JA, et al: Computed tomography of the urinary calculi. AJR 198 1;136:255258 5. Chait A, Matagan KW, Fabian CB, et al: Vascular impression on the ureters. AJR 1971;111:729-749 6. Coolsaet, BLRA: Ureteric pathology in relation to right and left gonadal veins. Urology 1978:12:4(X49 7. Kirks PR, Currarino G, Weinberg AG: Transverse

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folds in the proximal ureter: A normal variant in infants. AJR 1978; 130:463-464 8. Culp DA: Congenital anomalies of the ureter. In: Bergman H (ed): The Ureter (ed 2). New York: SpringerVerlag, 198 I ;644 9. Pollack HM, Popky GL, Blumberg ML: Hernias of the ureter and anatomic roentgenographic study. Radiology 1975;117:275-281 IO. Hyde I, Wastie ML: Striation (longitudinal mucosal folds) in the upper urinary tract. I. Striated renal pelvis and ureter. Br J Radio1 197 1;44:445-456 11. Culp DA: Congenital anomalies of the ureter. In: Bergman H (ed): The Ureter (ed 2). New York: SpringerVerlag, 198 1;644 12. Orr PS, McGregor CGA: Congenital ureteric cystrare anomaly. Virology 1978;12:699-700 13. Caine M: Diseases of the ureter. In: Bergman H (ed): The Ureter (ed 2). New York: Springer-Verlag, 198 1;199200 14. Reece RW, Koontz WW Jr: Leukoplakia of the urinary tract: A review. J Ural 1975;114:165-171 15. Willis JS, Pollack HM, Curtis JA: Cholesteatoma of the upper urinary tract. AJR 1981:136:941-944 16. Caine M: Diseases of the ureter. In: Bergman H (ed): The Ureter (ed 2). New York: Springer-Verlag, 1981;200 17. Elliot CB, Maloney PJ, Clement JC: Malacoplakia of the urinary tract. AJR 1972;116:830-837 18. Stomp B, Fallon B: Nonspecific granulomatous ureteritis. J Ural 1977;177:794-795 19. Caine M: Diseases of the ureter. in: Bergman H (ed): The Ureter (ed 2). New York: Springer-Verlag. 1981;201 20. Gerle RD: Roentgenographic features of primary renal candidiasis. Fungal ball of the renal pelvis and ureter. AJR 1973;119:731-738 21. Melchior J, Mehest WK, Volk WL: Ureteral colic from a fungus ball: Unusual presentation of systemic aspergillosis. J Ural 1972;108:698-699 22. Margolin HN: Fungus infections of the urinary tract. Sem Roentgen01 1971;6:323-330 23. Caine M: Diseases of the ureter. In: Bergman H (ed): The Ureter (ed 2). New York: Springer-Verlag, 1981;207214 24. Hanafy HM, Youssef TK, Saad SM: Radiological aspects of bilharzial (schistosomal) ureter. Urology 1975;6:118-124 25. Davidson AJ: Radiology of the kidney. Philadelphia: Saunders, 1985;193-199 26. Witten DM, Myers GH, Utz DC: Clinical Urography (ed 4). Philadelphia: Saunders, 1977;1554-1585. 27. Bergman H, Hotchkiss RS: Ureteral tumors. In: Bergman H (ed): The Ureter (ed 2). New York: Springer-Verlag, 1981;277 28. BergmanH, Hotchkiss RS: Ureteral tumors. In: Bergman H (ed): The Ureter (ed 2). New York: Springer-Verlag, 1981;272-274 29. Witten DM, Myers GH, Utz DC: Clinical Urography (ed 4). Philadelphia: Saunders, 1977;1582-1585 30. Witten DM, Myers GH, Utz DC: Clinical Urography (ed 4). Philadelphia: Saunders, 1977; 1572-l 582 3 1. Bergman H, Hotchkiss RS: Ureteral tumors. In: Berg-

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