DOI: 10.1148/rg.281075171
RadioGraphics 2008;28:255-276
Pyelonephritis: Radiologic-Pathologic Review1
William D. Craig, CDR, MC, USN,
Brent J. Wagner, MD, and
Mark D. Travis, LCDR, MC, USN
1 From the Department of Radiologic Pathology, Armed Forces Institute of Pathology, 6825 16th St, NW, Washington, DC 20306-6000 (W.D.C.); Department of Radiology and Radiological Sciences, Uniformed University of the Health Sciences, Bethesda, Md (W.D.C.); Department of Radiology, Reading Hospital and Medical Center, West Reading, Pa (B.J.W.); and the National Capitol Radiology Consortium, National Naval Medical Center, Bethesda, Md (M.D.T.). Received August 13, 2007; revision requested September 14 and received September 26; accepted September 28. All authors have no financial relationships to disclose.
Address correspondence to W.D.C. (e-mail: William.Craig{at}afip.osd.mil ).
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Abstract
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Urinary tract infections are the most common urologic disease in the United States and annually account for over 7 million office and 1 million emergency department visits. In adults, diagnosis of urinary tract infection is typically based on characteristic clinical features and abnormal laboratory values. Imaging is usually reserved for patients who do not respond to therapy and for those whose clinical presentation is either atypical or potentially life threatening. Urinary tract infection typically originates in the urinary bladder; when it migrates to the kidney or is seeded there hematogenously, a tubulointerstitial inflammatory reaction ensues, involving the renal pelvis and parenchyma. The condition is characterized as pyelonephritis. Complicated and uncomplicated pyelonephritis, xanthogranulomatous pyelonephritis, and tuberculosis are all urinary tract infections for which imaging evaluation adds diagnostic information important for patient care. Computed tomography (CT), when performed before, immediately after, and at delayed intervals from contrast material injection, is the preferred modality for evaluating acute bacterial pyelonephritis. CT is also preferred over conventional radiography and ultrasonography (US) for assessing emphysematous pyelonephritis. Xanthogranulomatous pyelonephritis is a chronic granulomatous process, induced by recurrent bacterial urinary tract infection. Although US is useful in the diagnosis of this condition, CT is the main imaging tool, as it provides highly specific findings and accurate assessment of the extrarenal extent of disease, which is essential for surgical planning. The increasing prevalence of tuberculosis and continued emergence of antibiotic-resistant strains have significance for genitourinary radiologists, as the urinary tract is the most common extrapulmonary site of tuberculosis. Familiarity with the renal manifestations of the disease—pelvoinfundibular strictures, papillary necrosis, cortical low-attenuation masses, scarring, and calcification—will help in the diagnosis, even in the absence of documented pulmonary disease.
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LEARNING OBJECTIVES
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After reading this article and taking the test, the reader will be able to:- Describe the pathophysiologic features associated with pyelonephritis and its complications in adults.
- Discuss the role of imaging in the evaluation of adult patients with suspected pyelonephritis.
- Identify the imaging features of pyelonephritis and its associated complications in adults.
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Introduction
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Urinary tract infections are the most common urologic disease in the United States and annually account for over 7 million office visits and 1 million emergency department visits (1). The direct and indirect costs of medical care for the infected individuals are enormous, approaching nearly $3 billion. Although women are more likely than men to experience urinary tract infections, both men and women are affected in large numbers. The anatomic structure of the urinary tract—an epithelium-lined tube with an opening at the body’s surface—makes this organ system susceptible to both symptomatic and asymptomatic colonization by infectious organisms, most commonly Escherichia coli. Fortunately, most of these infections are uncomplicated and involve only the urinary bladder. When infection migrates to the upper urinary tract or is seeded there hematogenously, both the renal pelvis and parenchyma become inflamed; thus, the condition is characterized as pyelonephritis (2,3). Pyelonephritis is but one cause of interstitial nephritis (4).
The role of diagnostic imaging in the evaluation of patients with suspected urinary tract infections has been much debated. 
In general, routine radiologic imaging is not required for diagnosis and treatment of uncomplicated cases in adult patients. When images are obtained, however, they demonstrate the nature and extent of disease and reveal complications such as abscess or obstruction. This article reviews the current understanding of the pathologic features of renal infection in adults, describes the role of diagnostic imaging, and correlates radiologic findings with the underlying disease process. The clinical, pathologic, and imaging features of both complicated and uncomplicated pyelonephritis are presented, along with a discussion of the granulomatous processes, tuberculosis and xanthogranulomatous pyelonephritis, and malacoplakia.
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Bacterial Pyelonephritis
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Clinical Features
For adult patients, urinary tract infections are typically diagnosed on the basis of their clinical symptoms and laboratory findings. Classic symptoms of pyelonephritis include an abrupt onset of chills, fever (temperature of 100°F or greater), and unilateral or bilateral flank pain with costovertebral tenderness. These "upper tract signs" are often accompanied by dysuria and urinary frequency and urgency (5). However, researchers are quick to point out that none of these symptoms is reliable for determining the anatomic level of infection. Furthermore, acute pyelonephritis may cause gastrointestinal symptoms, such as abdominal pain, nausea, vomiting, and diarrhea, which confound the diagnosis (5). Laboratory findings include pyuria, granular or leukocytic casts, bacteriuria, and a positive urine culture. Blood tests may show leukocytosis with a neutrophilic shift, elevated erythrocyte sedimentation rate, elevated C-reactive protein levels, and occasionally positive blood cultures that grow the same organism as cultured from the urine (5,6).
Immediately after the collection of urine for culture and antibiotic sensitivity testing, antibiotic therapy is started. Most patients respond successfully to antibiotics and do not require imaging studies or further intervention. In select clinical scenarios, however, diagnostic imaging plays a role, including (a) to assist in the diagnosis of acute pyelonephritis when the patient fails to respond to appropriate therapy within the first 72 hours (occurs in approximately 5% of patients), (b) to look for previously occult structural or functional abnormalities that may require intervention, (c) to assess those patients at significant risk for more severe life-threatening complications (eg, diabetic, elderly, or immunocompromised patients), (d) to characterize the severity of the infection to direct future therapy or interventions, and (e) to evaluate the extent of organ damage subsequent to a resolved acute infection. However, when imaging is performed, repeated follow-up is discouraged unless new clinical indications arise (1,7).
Pathologic Features
The pathophysiology of acute, ascending pyelonephritis is best discussed as a continuum of disease. The bladder is originally inoculated with an infectious organism, which then migrates up the ureter to the central collecting system. This ascent occurs even in the absence of reflux, owing to special virulence properties of the bacteria, such as the adhesin P fimbriae and endotoxins. The endotoxins are believed to inhibit ureteral peristalsis by blocking the 
-adrenergic nerves within smooth muscle, thus creating a functional obstruction. The obstruction compromises the forward flow of urine, which is a normal protective mechanism against upper urinary tract infection (5,8). An infected, inflamed ureter and renal pelvis are accurately characterized as ureteropyelitis and occasionally can be demonstrated radiologically before renal parenchymal changes evolve (Fig 1). Continuing their retrograde ascent, bacteria enter the renal tubules at the papillary tip and cause an inflammatory response that extends up the tubule and into the renal interstitium (10).
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Figure 1a. Unilateral pyelitis in a patient with suspected acute bacterial pyelonephritis. (a, b) Axial (a) and oblique reconstructed (b) images from contrast material–enhanced computed tomography (CT) demonstrate thickening and asymmetric enhancement of the central collecting system. (arrowhead). The overlying parenchyma enhances normally and appears radiologically normal. (c) Photomicrograph (original magnification, x200; hematoxylineosin stain) shows acute inflammation of the renal pyelocaliceal system and intense acute inflammation by polymorphonuclear leukocytes in the renal papillary tip, with erosion or loss of the overlying transitional epithelium (urothelium). (Reprinted, with permission, from reference 9.)
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Figure 1b. Unilateral pyelitis in a patient with suspected acute bacterial pyelonephritis. (a, b) Axial (a) and oblique reconstructed (b) images from contrast material–enhanced computed tomography (CT) demonstrate thickening and asymmetric enhancement of the central collecting system. (arrowhead). The overlying parenchyma enhances normally and appears radiologically normal. (c) Photomicrograph (original magnification, x200; hematoxylineosin stain) shows acute inflammation of the renal pyelocaliceal system and intense acute inflammation by polymorphonuclear leukocytes in the renal papillary tip, with erosion or loss of the overlying transitional epithelium (urothelium). (Reprinted, with permission, from reference 9.)
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Figure 1c. Unilateral pyelitis in a patient with suspected acute bacterial pyelonephritis. (a, b) Axial (a) and oblique reconstructed (b) images from contrast material–enhanced computed tomography (CT) demonstrate thickening and asymmetric enhancement of the central collecting system. (arrowhead). The overlying parenchyma enhances normally and appears radiologically normal. (c) Photomicrograph (original magnification, x200; hematoxylineosin stain) shows acute inflammation of the renal pyelocaliceal system and intense acute inflammation by polymorphonuclear leukocytes in the renal papillary tip, with erosion or loss of the overlying transitional epithelium (urothelium). (Reprinted, with permission, from reference 9.)
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Imaging Features
As an initial screening study, abdominal radiography is a rapid, inexpensive examination. Abdominal radiographs were routinely obtained as the first component of an excretory urographic study; however, use of CT has overtaken that of radiography in nearly all institutions. The scout radiographs were used to detect urinary tract gas and calcifications, but pitfalls included unreliable differentiation of abdominal bowel gas from urinary tract gas and nonvisualization of small urinary tract calcifications overlying normally ossified structures such as a transverse process. Excretory urography delineates the anatomy of the pelvicaliceal system and provides an overview of the urothelial system from the kidneys to the urinary bladder. Findings seen in cases of acute kidney infections include renal enlargement, striated or delayed nephrograms, delayed caliceal appearance time, and dilatation or effacement of the collecting system (Fig 2). The weaknesses of excretory urography include the inability to characterize masses (ie, as cysts, neoplasms, or abscesses), the lack of fine parenchymal detail, and the dependency on functioning kidneys. In addition, several studies have demonstrated that only about 25% of patients with acute pyelonephritis have abnormal findings at excretory urography (11, 12). Therefore, more advanced imaging techniques are generally preferred over excretory urography.
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Figure 2. Acute bacterial pyelonephritis of the left kidney. Tomogram from intravenous pyelography demonstrates an enlarged left kidney with effacement of the central collecting system.
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Ultrasonography (US) is occasionally used as a first-line diagnostic tool to evaluate the urinary tract in patients with symptoms of pyelonephritis. Unfortunately, interstitial nephritis is not well characterized in adults on routine gray-scale images. Therefore, most patients with clinically suspected pyelonephritis have negative results from US. In one prospective study, US demonstrated abnormalities in only 24% of patients; other studies reported percentages as low as 20% (13,14). When positive findings of pyelonephritis are found at US, they can include congenital anomalies and a variety of changes in the renal parenchyma such as hydronephrosis, renal enlargement, loss of renal sinus fat due to edema, changes in echogenicity due to both edema (hypoechoic) or hemorrhage (hyperechoic) (Fig 3) (15), loss of corticomedullary differentiation, abscess formation, and areas of hypoperfusion (visible with power Doppler interrogation). Even when positive US findings are observed, US is limited in the definitive differentiation of calcification from intraparenchymal or collecting system gas (manifested respectively as "clean" shadowing and "dirty" shadowing with echoes and reverberations), identification of perinephric extension of infection, and visualization of small microabscesses that are common in early acute infections (Fig 4) (16,17). Occasionally, areas of abnormal echogenicity can have a masslike appearance (Fig 5).
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Figure 3a. Acute bacterial pyelonephritis. (a) US scan shows a wedge-shaped hyperechoic focus (arrowhead) in the upper pole of the right kidney related to acute bacterial pyelonephritis. (b) Color flow US image demonstrates diminished flow through the involved area.
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Figure 3b. Acute bacterial pyelonephritis. (a) US scan shows a wedge-shaped hyperechoic focus (arrowhead) in the upper pole of the right kidney related to acute bacterial pyelonephritis. (b) Color flow US image demonstrates diminished flow through the involved area.
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Figure 4a. Severe unilateral acute bacterial pyelonephritis. (a) US image demonstrates a slightly enlarged right kidney that is otherwise unremarkable, belying the advanced disease. (b) CT scan shows the enlarged kidney with global decreased uptake of contrast material and multiple small low-attenuation foci from abscess pockets, findings that prompted nephrectomy. (c) Photograph of the resected gross specimen reveals multiple intrarenal abscesses that have begun to partially coalesce. Scale is in centimeters.
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Figure 4b. Severe unilateral acute bacterial pyelonephritis. (a) US image demonstrates a slightly enlarged right kidney that is otherwise unremarkable, belying the advanced disease. (b) CT scan shows the enlarged kidney with global decreased uptake of contrast material and multiple small low-attenuation foci from abscess pockets, findings that prompted nephrectomy. (c) Photograph of the resected gross specimen reveals multiple intrarenal abscesses that have begun to partially coalesce. Scale is in centimeters.
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Figure 4c. Severe unilateral acute bacterial pyelonephritis. (a) US image demonstrates a slightly enlarged right kidney that is otherwise unremarkable, belying the advanced disease. (b) CT scan shows the enlarged kidney with global decreased uptake of contrast material and multiple small low-attenuation foci from abscess pockets, findings that prompted nephrectomy. (c) Photograph of the resected gross specimen reveals multiple intrarenal abscesses that have begun to partially coalesce. Scale is in centimeters.
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Figure 5a. Masslike appearance of acute bacterial pyelonephritis. (a) US scan demonstrates a geographic, slightly lobulated "mass" (arrowhead) in the midpole of the left kidney, a finding that is worrisome for a solid tumor. (b) CT scan shows multifocal regions of diminished enhancement that extend to the periphery of the kidney, findings consistent with interstitial nephritis.
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Figure 5b. Masslike appearance of acute bacterial pyelonephritis. (a) US scan demonstrates a geographic, slightly lobulated "mass" (arrowhead) in the midpole of the left kidney, a finding that is worrisome for a solid tumor. (b) CT scan shows multifocal regions of diminished enhancement that extend to the periphery of the kidney, findings consistent with interstitial nephritis.
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The urinary bladder should always be imaged in a US evaluation for suspected pyelonephritis. Residual volumes of urine in the bladder after voiding can be calculated, and bladder wall thickness can be measured to estimate outflow obstruction. In male patients, the presence of prostate enlargement may be further supportive evidence of bladder outlet obstruction.
Newer applications of US such as tissue harmonic imaging have reported sensitivities and specificities as high as 97% and 80%, respectively (18). With tissue harmonic imaging, the parenchymal defects of pyelonephritis were commonly seen as focal or segmental, patchy, hypoechoic lesions extending from the medulla to the renal capsule. Kim et al (18) inferred that the same physiologic processes noted at CT—edema, tubular obstruction, and vasoconstriction—were demonstrated sonographically.
Scintigraphy performed with technetium 99m dimercaptosuccinic acid (a radiotracer excreted by means of tubular secretion and sometimes called a "tubular agent") provides high-resolution images of the renal cortex that allow for both qualitative and quantitative characterization of renal injury and impairment. Up to 90% of children with a febrile urinary tract infection have positive scintigraphic findings (19), including focal or global areas of diminished radiotracer uptake, as evidenced by photopenic defects within the parenchyma (Fig 6). Follow-up scintigraphy, which is usually performed at 6–12 months, provides a quantitative assessment of whether the disease is stable, progressing, or resolving. Occasionally, scintigraphy performed with radiolabeled white blood cells or gallium is used to locate renal infection, but infection cannot be definitively distinguished from sterile inflammation with any radiotracer. Furthermore, tubular agents cannot demonstrate perinephric spread of infection, and photopenic defects caused by acute infectious nephritis may be mischaracterized as scars if these scintigraphic studies are interpreted without the benefit of correlative imaging or comparison studies (19).
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Figure 6. Scintiscan obtained with technetium 99m dimercaptosuccinic acid demonstrates a photopenic, peripheral defect (arrow) in the upper lateral margin of the right kidney that correlates with an area of acute bacterial pyelonephritis.
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When imaging is warranted, CT is the modality of choice for evaluating acute bacterial nephritis. It provides comprehensive anatomic and physiologic information that accurately characterizes both intra- and extrarenal pathologic conditions. Unenhanced CT is excellent for identifying urinary tract gas, calculi, hemorrhage, renal enlargement, inflammatory masses, and obstruction (Figs 7, 8) (20). Involved regions occasionally appear with lower attenuation related to edema; less frequently, they have pockets of higher attenuation that are thought to represent hemorrhage (15).
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Figure 7. Acute bacterial pyelonephritis. (7) Unenhanced CT scan from a clinically documented case of acute bacterial pyelonephritis shows asymmetric enlargement and absence of the pyramids of the right kidney (cf the preserved pyramids [arrow] in the normal left kidney). Loss of the renal pyramids is a nonspecific marker for edema, which is more typically seen in obstruction related to calculi.
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Figure 8. Acute bacterial pyelonephritis. (8) Unenhanced CT scan demonstrates multiple, scattered, round and oval hyperattenuation foci within the left kidney, findings indicative of hemorrhagic acute bacterial pyelonephritis.
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The above findings are frequently absent, however, and unenhanced CT images may appear normal. It is only after contrast material is administered that the diagnostic features of acute bacterial nephritis are revealed. A reasonable protocol for CT in suspected cases of acute pyelonephritis was recently published. The authors recommend precontrast imaging (ie, before contrast material administration) followed by postcontrast imaging at approximately 50–90 seconds after injection and delayed imaging only if urinary tract obstruction is suspected (6). These parameters are designed to take advantage of the nephrographic phase in which the normal kidney is homogeneously enhanced. After administration of contrast material, acute bacterial nephritis most commonly manifests as one or more wedge-shaped areas or streaky zones of lesser enhancement that extend from the papilla to the renal cortex. This pattern of differential enhancement reflects the underlying pathophysiology of tubular obstruction caused by inflammatory debris within the lumen, interstitial edema, and vasospasm (Fig 9) (10). All three of these pathophysiologic disturbances tend to decrease the flow of contrast agent through the tubule, which also helps explain the pattern of delayed and persistent enhancement seen 3–6 hours after administration of contrast material. The sites that originally demonstrated reduced attenuation during the nephrographic phase transmute from hypoattenuation to hyperattenuation wedge-shaped defects because of the prolonged accumulation of contrast agent that slowly transits the compromised tubules (Fig 10) (21).
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Figure 9a. Acute bacterial nephritis. (a) Photograph of the cut surface of a resected kidney shows a wedge-shaped, lighter region of renal cortex that represents acute bacterial nephritis. (b) Contrast-enhanced CT scan demonstrates decreased enhancement throughout the same area. Note the sharp transition (arrowhead) between normal and abnormal kidney. (c) Photomicrograph (original magnification, x400; hematoxylineosin stain) shows a duct (arrowhead) that contains a cast of polymorphonuclear lymphocytes. Pus casts may be seen in the urine of patients with acute bacterial pyelonephritis. (Figs 9a and 9c reprinted, with permission, from reference 9.)
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Figure 9b. Acute bacterial nephritis. (a) Photograph of the cut surface of a resected kidney shows a wedge-shaped, lighter region of renal cortex that represents acute bacterial nephritis. (b) Contrast-enhanced CT scan demonstrates decreased enhancement throughout the same area. Note the sharp transition (arrowhead) between normal and abnormal kidney. (c) Photomicrograph (original magnification, x400; hematoxylineosin stain) shows a duct (arrowhead) that contains a cast of polymorphonuclear lymphocytes. Pus casts may be seen in the urine of patients with acute bacterial pyelonephritis. (Figs 9a and 9c reprinted, with permission, from reference 9.)
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Figure 9c. Acute bacterial nephritis. (a) Photograph of the cut surface of a resected kidney shows a wedge-shaped, lighter region of renal cortex that represents acute bacterial nephritis. (b) Contrast-enhanced CT scan demonstrates decreased enhancement throughout the same area. Note the sharp transition (arrowhead) between normal and abnormal kidney. (c) Photomicrograph (original magnification, x400; hematoxylineosin stain) shows a duct (arrowhead) that contains a cast of polymorphonuclear lymphocytes. Pus casts may be seen in the urine of patients with acute bacterial pyelonephritis. (Figs 9a and 9c reprinted, with permission, from reference 9.)
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Figure 10. Acute bacterial pyelonephritis. Delayed phase CT scan obtained through the midpole of the right kidney demonstrates an intense persistent nephrogram (arrowhead) around the posterior rim of the kidney along two medullary rays.
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In acute bacterial nephritis, the alternating bands of hypo- and hyperattenuation, which correspond to differential enhancement of infected and noninfected parenchyma, are sharply defined. Over time, the differential enhancement becomes less distinct and ultimately will either completely normalize or evolve to scar, as evidenced by loss of parenchymal volume.
When round, peripheral hypoattenuation renal lesions are seen in the clinical setting of pyelonephritis, hematogenous seeding should be considered (Fig 11) (10,22). Blood and urine cultures that grow organisms associated with skin or oral flora, such as Staphylococcus or Streptococcus species, support the hypothesis of hematogenous infection. However, when the lesions generalize within the kidney or coalesce, differentiating between ascending and hematogenous infection may not be possible (23,24). Occasionally, these CT findings are identified in the absence of clinically suspected pyelonephritis and are mistaken for multiple neoplastic masses, a misdiagnosis that may prompt unnecessary surgical consultation and biopsy requests.
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Figure 11. Acute bacterial pyelonephritis caused by hematologic seeding in a patient with Staphylococcus aureus endocarditis. CT scan demonstrates peripheral low-attenuation lesions (arrowheads) that are maturing into small abscess cavities. In such cases, blood and urine cultures grow the same organism.
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The healing process, as seen radiologically, lags behind clinical improvement. With appropriate antibiotic therapy, urine specimens usually become sterile within a few hours. In most patients, fever abates in 24–48 hours, and patients are considered clinically cured within 4–5 days. However, the imaging abnormalities are reported to heal over 1–5 months, and the delay in healing correlates best with persistent pyuria. The persistent urinary leukocytes imply residual inflammation that can usually be detected with CT (24,25).
Infection is only one cause of interstitial nephritis. The inflammation can be induced by drugs, granulomatous diseases, metabolic disorders, and immunologically mediated mechanisms (Fig 12) (4). These other entities are much less common than acute bacterial nephritis; thus, in the appropriate clinical setting, it is reasonable to assume that the characteristic findings of interstitial nephritis are caused by infection.
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Figure 12. Sarcoidosis. CT scan shows multiple geographic hypoattenuation regions throughout both kidneys that are related to the patient’s sarcoidosis. The defects are indistinguishable from those caused by pyelonephritis, the most commonly imaged interstitial nephritis.
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CT is also the best modality for fully evaluating the secondary signs of renal inflammatory disease and its complications. These signs include focal or global enlargement of the kidney, perinephric stranding, thickening of Gerota fascia, and abscess formation (Fig 13) (11,17,20,26,27).
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Figure 13a. Intrarenal abscess with perinephric extension. (a) CT scan demonstrates an abscess cavity with a peripheral enhancing rim but no central enhancement in the right kidney. (b) Delayed phase CT scan shows secondary signs that include delayed clearance of contrast material as evidenced by asymmetric visualization of the enhanced pyramids (arrow), stranding throughout the perinephric space, and thickening of Gerota fascia (arrowhead).
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Figure 13b. Intrarenal abscess with perinephric extension. (a) CT scan demonstrates an abscess cavity with a peripheral enhancing rim but no central enhancement in the right kidney. (b) Delayed phase CT scan shows secondary signs that include delayed clearance of contrast material as evidenced by asymmetric visualization of the enhanced pyramids (arrow), stranding throughout the perinephric space, and thickening of Gerota fascia (arrowhead).
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Abscess cavities may be either intra- or extra-parenchymal, and a renal abscess should be suspected when appropriate therapy does not lead to clinical response. Diabetic patients are predisposed to abscess formation, with 75% of all renal abscesses occurring in this patient population. Interestingly, up to 15%–20% of patients with an abscess have negative urine cultures (28). This observation may reflect the fact that the infection has been relatively contained within a focal process.
At CT, abscesses are typically identified as round or geographic low-attenuation collections that do not enhance centrally but that may have an enhancing rim. The rims are pseudocapsules with varied wall thicknesses and frequent nodularity. A halo of diminished enhancement may surround the abscess during the nephrographic phase. Extraparenchymal collections occasionally extend into adjacent structures, such as the psoas muscle (Fig 13).
At US, the typical abscess appears as a hypoechoic mass with through transmission that lacks internal flow on color Doppler flow images (Fig 14). Occasionally, mobile debris may be seen within the collection and should not be misinterpreted as true vascular flow at color Doppler analysis (24).
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Figure 14a. Early and mature abscess cavities. (a) US scan demonstrates a geographic hypoechoic focus from an abscess in the upper pole of the right kidney. (b) On a US scan of a more mature abscess, the cavity is better defined, with a visible pseudocapsule and through transmission that is evidenced by increased echogenicity deep to the upper pole lesion.
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Figure 14b. Early and mature abscess cavities. (a) US scan demonstrates a geographic hypoechoic focus from an abscess in the upper pole of the right kidney. (b) On a US scan of a more mature abscess, the cavity is better defined, with a visible pseudocapsule and through transmission that is evidenced by increased echogenicity deep to the upper pole lesion.
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MR imaging of renal infections continues to gain acceptance. It is especially useful in patients for whom exposure to radiation should be avoided (eg, pregnant patients) or for whom use of iodinated contrast material is contraindicated (eg, patients with a sensitivity to iodinated contrast agents). MR imaging findings are similar to those of CT and include demonstration of renal edema, hemorrhage, renal enlargement, abscesses, and perinephric fluid collections (29). Inflammatory lesions and fluid collections generally follow the expected signal intensity pattern of simple fluid (ie, low intensity on T1-weighted images and high intensity on T2-weighted images). Most radiologists consider pregnancy to represent a contraindication to the use of gadolinium-based contrast material. In nonpregnant patients, following intravenous administration of gadolinium, both wedge-shaped and striated areas of decreased enhancement can be seen (29,30). Conspicuity of intrarenal lesions can be augmented by obtaining gadolinium-enhanced inversion recovery images. This protocol takes advantage of the negative enhancement effects of gadolinium. The tubular obstruction and edema within the involved region translates into decreased levels of gadolinium. These involved regions do not accumulate sufficient gadolinium to lead to a signal drop and therefore stand out in relief against the normally perfused kidney, which becomes hypointense after the administration of contrast agent (26,30) (Fig 15). In cases in which the collecting system is dilated, concurrent MR urography could easily be performed to look for anatomic obstruction. One potential pitfall is the presence of calculi or gas, both of which are problematic with respect to magnetic susceptibility artifact and unpredictable characterization with MR imaging.
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Figure 15. MR imaging of acute bacterial pyelonephritis. Sagittal short inversion-time inversion recovery image of the right kidney obtained after gadolinium administration demonstrates signal drop off in the normal middle and lower renal poles due to normal perfusion and uptake of contrast agent. The infected upper pole, with its compromised perfusion, remains bright (arrowhead) and stands out in relief. (Courtesy of Gael J. Lonergan, MD, Dell Children’s Hospital, Austin, Tex.)
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Chronic Pyelonephritis
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Chronic pyelonephritis is a somewhat controversial disease from a pathogenetic standpoint. Despite the ongoing debate on whether the condition is an active chronic infection, arises from multiple recurrent infections, or represents stable changes from a remote single infection, its radiologic appearance is the same. The imaging findings are characterized by renal scarring, atrophy and cortical thinning, hypertrophy of residual normal tissue (which may mimic a mass lesion), caliceal clubbing secondary to retraction of the papilla from overlying scar, thickening and dilatation of the caliceal system, and overall renal asymmetry (Fig 16). Hypertension is frequently a long-term sequela (1). It is important to note that once the radiologic changes of chronic pyelonephritis have been established, repeat imaging is unlikely to provide evidence of new findings.
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Figure 16a. Chronic pyelonephritis. (a) Unenhanced CT scan shows a small, deformed right kidney with multiple deep scars and dystrophic calcifications. (b) Photograph of the resected kidneys demonstrates extensive bilateral scar formation. (Reprinted, with permission, from reference 9.)
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Figure 16b. Chronic pyelonephritis. (a) Unenhanced CT scan shows a small, deformed right kidney with multiple deep scars and dystrophic calcifications. (b) Photograph of the resected kidneys demonstrates extensive bilateral scar formation. (Reprinted, with permission, from reference 9.)
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Emphysematous Pyelonephritis
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Clinical Features
Emphysematous pyelonephritis is a life-threatening necrotizing infection of the kidneys characterized by gas formation within or surrounding the kidneys. The majority (approximately 90%) of patients have poorly controlled diabetes. Nondiabetic patients are typically either immunocompromised or have associated urinary tract obstruction secondary to uroliths, neoplasm, or sloughed papilla. The most commonly identified organisms are E coli, Klebsiella pneumonia, and Proteus mirabilis (1,16). Without early therapeutic intervention, the condition becomes rapidly progressive, generalizes to fulminant sepsis, and carries a high mortality rate.
Imaging Features
Conventional radiography demonstrates either mottled gas within the renal fossa or crescentic collections of gas within the Gerota fascia (a finding indicative of infection extending into the perinephric spaces) (Fig 17). Abnormal collections of gas are seen in about 70% of patients (31).
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Figure 17. Bilateral emphysematous pyelonephritis. Abdominal radiograph from an intravenous pyelographic study demonstrates lucent air that outlines both kidneys (arrowheads). Gas has also escaped into the retroperitoneum and appears in linear collections along the left paraspinous region (arrow).
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US demonstrates an enlarged kidney with high-amplitude, nondependent echoes within the renal parenchyma or collecting system (16,31) (Fig 18). The echogenic foci appear different than those seen in typical stone disease, with the distal shadowing having reverberations and low-level echoes that are nicknamed "dirty shadowing." Confounding factors in a US evaluation of this disease are the presence of adjacent bowel gas or calculi, which may cause confusion and interpretive errors. Furthermore, US is poor for correctly categorizing which type of emphysematous pyelonephritis is present (31).
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Figure 18a. Emphysematous pyelonephritis. (a) US image shows nondependent echoes within the left kidney that demonstrate a ring-down artifact. (b) Corresponding CT scan helps confirm that this pattern is caused by intraparenchymal air.
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Figure 18b. Emphysematous pyelonephritis. (a) US image shows nondependent echoes within the left kidney that demonstrate a ring-down artifact. (b) Corresponding CT scan helps confirm that this pattern is caused by intraparenchymal air.
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CT is the modality of choice for evaluating patients with emphysematous pyelonephritis. The type of emphysematous pyelonephritis can be easily and accurately defined on the basis of CT findings (31). Findings include parenchymal enlargement and destruction, small bubbly or linear streaks of gas, fluid collections, gas-fluid levels, and focal tissue necrosis with or without abscess (31,32).
Two types of distribution of the gas have been found to correlate with prognosis. Type 1 emphysematous pyelonephritis is characterized by renal parenchymal destruction that manifests with either streaky or mottled areas of gas. Intra- or extrarenal fluid collections are notably absent (Fig 19a). In contradistinction, type 2 emphysematous pyelonephritis is characterized by renal or perirenal fluid collections that are directly associated with bubbly or loculated gas or by gas within the urinary collecting system (Fig 19b). Type 1 disease has a more aggressive clinical course, with a shorter interval between initial presentation and death. Wan et al (31), who defined these two types, suggested that the differences in patient outcome relate to disparities in the severity of immunocompromise in type 1 versus type 2 patients or to vascular insufficiency of the involved kidney. They reported mortality rates of 69% for patients with type 1 disease and 18% for patients with type 2 disease (31). However, more recent literature that advocates aggressive medical treatment along with percutaneous drainage and partial or complete nephrectomy reported much better results. Mortality rates for both types were both approximately 8% (33).
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Figure 19a. Types 1 and 2 emphysematous pyelonephritis. (a) Unenhanced CT scan demonstrates type 1 emphysematous pyelonephritis, which appears as a large area of air that has completely destroyed and distorted the right kidney. Note the absence of fluid within or around the kidney. (b) Unenhanced CT scan of type 2 emphysematous pyelonephritis shows air within both the renal parenchyma and the collecting system, with associated fluid collections along the lateral border.
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Figure 19b. Types 1 and 2 emphysematous pyelonephritis. (a) Unenhanced CT scan demonstrates type 1 emphysematous pyelonephritis, which appears as a large area of air that has completely destroyed and distorted the right kidney. Note the absence of fluid within or around the kidney. (b) Unenhanced CT scan of type 2 emphysematous pyelonephritis shows air within both the renal parenchyma and the collecting system, with associated fluid collections along the lateral border.
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Emphysematous Pyelitis
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Emphysematous pyelitis is a less aggressive form of emphysematous infection of the upper urinary tract. Emphysematous pyelitis is diagnosed when gas is localized to the renal collecting system. Emphysematous pyelitis is more common in women and is also associated with diabetes and urinary tract obstruction. The overall mortality rate is significantly less than that for emphysematous pyelonephritis (1,32). Noninfectious sources of air (eg, trauma, instrumentation, and fistula) should be excluded.
In emphysematous pyelitis, radiography demonstrates gas in the outline of the ureters and the dilated calices. US findings are typically nondependent high-amplitude flat echoes within the renal sinus or calices that represent the foci of air. CT findings are a dilated collecting system, gas bubbles or gas-fluid levels within the renal caliceal system or renal sinus, and the lack of parenchymal gas (Fig 20). Use of CT allows accurate differentiation of emphysematous pyelitis from emphysematous pyelonephritis (17,32).
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Figure 20a. Emphysematous pyelitis. CT images of the abdomen (a) and pelvis (b) demonstrate bilateral collections of air within the central collecting systems (arrowhead in a) and along each ureter (arrowheads in b).
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Figure 20b. Emphysematous pyelitis. CT images of the abdomen (a) and pelvis (b) demonstrate bilateral collections of air within the central collecting systems (arrowhead in a) and along each ureter (arrowheads in b).
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Pyonephrosis
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Clinical Features
Pyonephrosis is simply an infected and obstructed collecting system, which frequently is enlarged. In the adult population, the obstruction may arise from a variety of disease processes such as calculi, tumor, complications from pyelonephritis (sloughed papilla), or strictures. Early diagnosis is crucial because direct, immediate intervention is required in these patients. If pyonephrosis is left untreated, a rapid, often permanent, decline in renal function may result, and patients not uncommonly develop septic shock (34,35). Pyonephrosis should be suspected in any patient with a known urinary tract obstruction and accompanying fever and flank pain. However, patients also present with more subtle clinical signs (weight loss and dull pain); uncommonly (15% of cases), they have no symptoms at all (35).
Imaging Features
US can be used to look for dilatation of the pelvicaliceal system, echogenic collecting system debris, fluid-fluid levels within the collecting system, and occasionally the incomplete (dirty) echoes of collecting system gas (34–37). Echogenic debris (ie, the lack of a completely anechoic collecting system) is the most reliable sign of pyonephrosis (36,37) (Fig 21). These signs can provide a sensitivity of 90%, specificity of 97%, and accuracy of 96% in the diagnosis of pyonephrosis versus simple hydronephrosis (34).
CT demonstrates thickening of the renal pelvic wall (>2 mm), parenchymal or perinephric inflammatory changes, dilatation and obstruction of the collecting system, higher than usual attenuation values of the fluid within the renal collecting system, and layering of contrast material above and anterior to the purulent fluid on excretory studies (27,34,35,38). A caveat to CT evaluation is that it is often difficult to distinguish simple hydronephrosis from pyonephrosis on the basis of fluid attenuation measurements (38).
MR imaging demonstrates findings similar to those seen at CT in pyonephrosis. Dilated pelvicaliceal system, debris within the system, and fluid-fluid levels are often present (20). Some preliminary promising work has been done with both diffusion-weighted imaging and apparent diffusion coefficient maps in an attempt to distinguish hydronephrosis from pyonephrosis, but these techniques require further investigation (39).
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Xanthogranulomatous Pyelonephritis
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Clinical Features
Xanthogranulomatous pyelonephritis is a chronic destructive granulomatous process that is believed to result from an atypical, incomplete immune response to subacute bacterial infection. Most patients have no specific risk factors, although diabetes mellitus is seen in approximately 10% of patients (40). Female patients are more frequently affected than male patients in a ratio of 2:1, and, although the disease most commonly occurs in middle age, both children and the elderly may be afflicted. Symptoms are often nonspecific (low-grade fever and malaise), but flank pain and hematuria may help direct the clinical and imaging evaluation to the urinary tract. In a recent series of 26 cases, over 95% had pyuria and over 60% had positive urine cultures (41); prior studies reported similar observations (42). In an early series of 18 cases, hematuria was present in 22% (40).
Pathologic Features
Xanthogranulomatous pyelonephritis is a chronic granulomatous process, induced by recurrent bacterial urinary tract infection, in which the renal parenchyma is ultimately replaced with lipid-laden (foamy) macrophages. Most cases occur in association with a renal pelvic calculus, and, consequently, hydronephrosis is thought to be a contributing factor. Ultimately, however, the loss of renal function and the destruction of the renal parenchyma are based on severe diffuse inflammation rather than obstruction. The most common organisms implicated are P mirabilis and E coli, but a variety of other bacteria may be found. The etiologic factors that precipitate development of xanthogranulomatous pyelonephritis in a small fraction of patients suffering from more common forms of renal infection are unknown. At microscopic examination, the caliceal mucosa is ulcerated and replaced by necrotic debris with numerous inflammatory cells, particularly polymorphonuclear leukocytes. The adjacent tissue layer consists of granulation tissue with lipid-laden macrophages that may be multinucleated. The inflammatory zone is associated with a predominantly plasma cellular infiltrate and is bordered by a band of fibrous tissue (42).
Imaging Features
Before the widespread use of cross-sectional imaging, a preoperative diagnosis of xanthogranulomatous pyelonephritis was possible in only a small percentage of patients. The radiographic finding of a large staghorn calculus is present in most, but not all, cases (Fig 22). However, this finding by itself is nonspecific and is not typically associated with the extensive inflammatory process that characterizes xanthogranulomatous pyelonephritis. Additional radiographic findings include enlargement of the renal outline and, with more advanced disease, obscuration of the ipsilateral psoas margin. When the evaluation includes excretory urography, a pronounced decrease in renal function on the affected side is observed, usually with no excretion despite delayed imaging. Again, the finding is not specific, as it may be seen with severe hydronephrosis (especially when chronic and associated with severe cortical loss) (40,42).
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Figure 22. Xanthogranulomatous pyelonephritis with staghorn calculus. Abdominal radiograph shows a classic staghorn calculus secondary to xanthogranulomatous pyelonephritis in the location of the right kidney.
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US typically demonstrates an enlarged kidney, with a large amorphous central echogenicity that corresponds to a renal pelvis staghorn calculus. The calculus is generally associated with acoustic shadowing. A loss of normal renal architecture is seen in most cases, but, because the disease is usually diffuse, a discrete inflammatory mass is uncommon. Although the US findings in diffuse xanthogranulomatous pyelonephritis are characteristic, US is usually followed by CT for definitive assessment.
CT is the mainstay of diagnostic imaging for xanthogranulomatous pyelonephritis for two reasons: (a) The majority of cases demonstrate a highly specific set of findings that allow a confident diagnosis and (b) surgical planning depends on the accurate assessment of the extrarenal extent of disease, if any. The combination of a nonfunctioning enlarged kidney, a central calculus within a contracted renal pelvis, expansion of the calices, and inflammatory changes in the perinephric fat is strongly suggestive of xanthogranulomatous pyelonephritis (Fig 23). Although the branching area of hypoattenuation extending from the contracted renal pelvis may suggest hydronephrosis, the low attenuation corresponds to an extensive inflammatory infiltrate rather than fluid in almost all cases (and percutaneous nephrostomy is not performed in most instances). Renal function (excretion) is rarely seen at the time of diagnosis, although variable rim enhancement surrounding the central branching inflammatory process is common.
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Figure 23a. Xanthogranulomatous pyelonephritis. (a) Contrast-enhanced CT scan demonstrates bilateral staghorn calculi, with distention of the right collecting system secondary to inflammatory debris. (b) US scan also shows the dilated collecting system (arrowheads) and a shadowing calculus (arrow). (c) Photograph of a cut specimen clearly depicts a complex, milky infiltrate that fills and expands the collecting system.
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Figure 23b. Xanthogranulomatous pyelonephritis. (a) Contrast-enhanced CT scan demonstrates bilateral staghorn calculi, with distention of the right collecting system secondary to inflammatory debris. (b) US scan also shows the dilated collecting system (arrowheads) and a shadowing calculus (arrow). (c) Photograph of a cut specimen clearly depicts a complex, milky infiltrate that fills and expands the collecting system.
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Figure 23c. Xanthogranulomatous pyelonephritis. (a) Contrast-enhanced CT scan demonstrates bilateral staghorn calculi, with distention of the right collecting system secondary to inflammatory debris. (b) US scan also shows the dilated collecting system (arrowheads) and a shadowing calculus (arrow). (c) Photograph of a cut specimen clearly depicts a complex, milky infiltrate that fills and expands the collecting system.
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Of 29 patients from two separate CT series, 28 had evidence of significant extrarenal extent, although a more recent series of 11 patients showed extrarenal disease in less than half of the cases (40,43,44). Psoas abscess and fistula formation (which is often cutaneous or colonic) are among the more clinically significant patterns of disease progression (40,45).
Although less common, the atypical manifestations of xanthogranulomatous pyelonephritis merit discussion. Specifically, the process is focal in approximately 10% of patients (Fig 24). Some of these cases are related to a duplicated collecting system and demonstrate findings similar to those seen in the diffuse form (with sparing of the upper or lower pole moiety), but others more closely mimic the features of bacterial abscess. In the latter cases, the findings, combined with the often subacute clinical presentation, do not allow easy differentiation from neoplasm.
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Figure 24a. Focal xanthogranulomatous pyelonephritis. (a) Contrast-enhanced CT scan demonstrates a thick-walled, peripherally enhancing, low-attenuation lesion. (b) Coronal contrast-enhanced T1-weighted MR image demonstrates the lesion with very similar characteristics. (c) Photograph of the cut specimen shows the thick-walled, yellowish capsule of the focal lesion. (d) Photomicrograph (original magnification, x400; hematoxylineosin stain) shows a large collection of foamy macrophages and histiocytes (arrowhead). (Reprinted, with permission, from reference 9.)
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Figure 24b. Focal xanthogranulomatous pyelonephritis. (a) Contrast-enhanced CT scan demonstrates a thick-walled, peripherally enhancing, low-attenuation lesion. (b) Coronal contrast-enhanced T1-weighted MR image demonstrates the lesion with very similar characteristics. (c) Photograph of the cut specimen shows the thick-walled, yellowish capsule of the focal lesion. (d) Photomicrograph (original magnification, x400; hematoxylineosin stain) shows a large collection of foamy macrophages and histiocytes (arrowhead). (Reprinted, with permission, from reference 9.)
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Figure 24c. Focal xanthogranulomatous pyelonephritis. (a) Contrast-enhanced CT scan demonstrates a thick-walled, peripherally enhancing, low-attenuation lesion. (b) Coronal contrast-enhanced T1-weighted MR image demonstrates the lesion with very similar characteristics. (c) Photograph of the cut specimen shows the thick-walled, yellowish capsule of the focal lesion. (d) Photomicrograph (original magnification, x400; hematoxylineosin stain) shows a large collection of foamy macrophages and histiocytes (arrowhead). (Reprinted, with permission, from reference 9.)
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Figure 24d. Focal xanthogranulomatous pyelonephritis. (a) Contrast-enhanced CT scan demonstrates a thick-walled, peripherally enhancing, low-attenuation lesion. (b) Coronal contrast-enhanced T1-weighted MR image demonstrates the lesion with very similar characteristics. (c) Photograph of the cut specimen shows the thick-walled, yellowish capsule of the focal lesion. (d) Photomicrograph (original magnification, x400; hematoxylineosin stain) shows a large collection of foamy macrophages and histiocytes (arrowhead). (Reprinted, with permission, from reference 9.)
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Another atypical feature is renal atrophy (rather than enlargement). Although not characteristic, renal atrophy was observed in five of 13 patients in one series (44).
Calculi are absent in up to 10% of cases (including the diffuse form). Gas is rarely seen and may be confused with pyonephrosis or emphysematous pyelonephritis.
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Tuberculosis
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Clinical Features
The increasing prevalence of tuberculosis in developed countries is well established and at least partly arises from both the spread of human immunodeficiency viral (HIV) infection and the continued emergence of mycobacterial strains with resistance to standard antibiotic therapy. The most common extrapulmonary site of tuberculosis is the urinary tract, with almost all cases resulting from hematogenous seeding. Despite the presumed route of spread from the lungs to the kidney, less than 50% of patients in whom urinary tract tuberculosis is ultimately diagnosed have abnormal results from chest radiography. Symptoms are often nonspecific (low-grade fever, malaise, or weakness). Hematuria and culture-negative pyuria may be seen at urinalysis (46).
Pathologic Features
After the tubercle bacilli reach the kidney, granulomas form and remain indolent for many years (Fig 25). If reactivation occurs, the infection spreads into the medulla, with direct involvement of the papillae (46). Further extension to the collecting system, with the potential for fibrosis, often occurs. Patients with untreated renal tuberculosis may totally lose renal function, and the disease may extend across retroperitoneal fascial planes to involve adjacent organs including the colon.
Imaging Features
Imaging findings of renal tuberculosis result from the combination of papillary necrosis and parenchymal destruction (Fig 26). The latter typically involves the papillae initially, but cortical damage soon follows. The collecting system demonstrates thickening, ulceration, and fibrosis (often with stricture formation) (46–48). The combination of this deterioration with papillary necrosis (manifested by a dilated calix and attenuated papillae) is very suggestive of tuberculosis (Fig 27). Stricture formation may result in focal non-excretion ("phantom calix" formation). The collecting system is distorted to some degree in the vast majority of patients with renal tuberculosis. This distortion results not only from irregular stricture formation but also from cavity formation, which arises from parenchymal necrosis, that may communicate with the collecting system. As the parenchymal lesions evolve, scarring (both medullary and cortical) produces irregular abnormalities in the renal contour, although the diseased kidney generally maintains a vaguely reniform shape.
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Figure 26a. Papillary necrosis related to tuberculosis. (a–c) Photographs of a cut gross specimen show the early necrosis of the medullary tip (black spot in a). Once devitalized, the papilla sloughs off, leaving a defect (cavity in b) within the medulla that is retrievable (necrotic tissue in c). (d) Collimated image from intravenous urography demonstrates multiple papillary cavities.
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Figure 26b. Papillary necrosis related to tuberculosis. (a–c) Photographs of a cut gross specimen show the early necrosis of the medullary tip (black spot in a). Once devitalized, the papilla sloughs off, leaving a defect (cavity in b) within the medulla that is retrievable (necrotic tissue in c). (d) Collimated image from intravenous urography demonstrates multiple papillary cavities.
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Figure 26c. Papillary necrosis related to tuberculosis. (a–c) Photographs of a cut gross specimen show the early necrosis of the medullary tip (black spot in a). Once devitalized, the papilla sloughs off, leaving a defect (cavity in b) within the medulla that is retrievable (necrotic tissue in c). (d) Collimated image from intravenous urography demonstrates multiple papillary cavities.
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Figure 26d. Papillary necrosis related to tuberculosis. (a–c) Photographs of a cut gross specimen show the early necrosis of the medullary tip (black spot in a). Once devitalized, the papilla sloughs off, leaving a defect (cavity in b) within the medulla that is retrievable (necrotic tissue in c). (d) Collimated image from intravenous urography demonstrates multiple papillary cavities.
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Figure 27. Tuberculosis. Retrograde pyelogram shows that the upper pole calix is stenotic (arrow) with associated papillary necrosis. The adjacent calix is fibrotic and distorted as well.
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Calcification is present in a large number (40%–70%) of cases (49). The extent of calcification ranges from thin rims surrounding low-attenuation areas of focal cortical inflammation to diffuse uniformly radiodense areas that extensively replace portions or all of the renal parenchyma ("autonephrectomy") in late-stage disease (Fig 28).
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Figure 28a. Calcifications of tuberculosis. (a) Abdominal radiograph demonstrates extensive calcifications forming a cast of the kidney and ureter. (b) Photograph of the cut specimen shows complete replacement of the normal kidney by inflammatory debris.
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Figure 28b. Calcifications of tuberculosis. (a) Abdominal radiograph demonstrates extensive calcifications forming a cast of the kidney and ureter. (b) Photograph of the cut specimen shows complete replacement of the normal kidney by inflammatory debris.
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The findings described above (pelvoinfundibular strictures, papillary necrosis, cortical low-attenuation masses, scarring, and calcification) may be seen in other conditions, but the combination of three or more of these findings is highly suggestive of tuberculosis (46), even in the absence of documented pulmonary disease.
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Malacoplakia
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Clinical Features
Malacoplakia is a rare, inflammatory process related to an abnormal host response to chronic infection. The condition most commonly affects the urinary bladder, but any urotheliallined location can be involved, and malacoplakia is occasionally seen outside the genitourinary tract, including in the gastrointestinal tract and skin (50). Middle-aged women, who constitute the demographic group most susceptible to recurrent urinary tract infections, develop malacoplakia at a rate three to four times greater than their male counterparts. The most frequently recovered organism is E coli (51). Patients present with hematuria or irritative bladder symptoms, such as dysuria and urinary urgency and frequency. Patients with advanced disease may present with renal failure. The prevalence of malacoplakia peaks in patients in the fifth decade of life, but the disease occasionally occurs in children. The process is also associated with immunosuppression and is encountered more frequently in patients with HIV infection or acquired immunodeficiency syndrome, those with other autoimmune diseases, or transplant recipients (52).
Pathologic Features
Malacoplakia is a nonneoplastic, space-occupying process that is thought to represent altered intracellular processing of ingested organisms by histiocytes (4). The first cases were reported in 1902 by Michaelis and Gutmann, who identified unusual intracellular inclusion bodies (the eponymic Michaelis-Gutmann bodies) in large eosinophilic macrophages (Hansemann histiocytes) present within tumorlike lesions of the genitourinary system (53). These intracellular inclusion bodies represent phagocytosed bacterial elements and are the signature histologic finding of malacoplakia (26).
Imaging Features
Because malacoplakia most commonly manifests as a mucosal mass involving the bladder or ureter, the most frequent renal finding is obstruction secondary to a lesion in the lower tract (54). However, when the kidney is directly involved, an infiltrative multifocal process is typically observed. Unlike malacoplakia of the bladder, renal involvement is progressive, nephrotoxic, and potentially lethal. In approximately 15% of reported cases, the kidney is identified as the primary site of disease (51). Lesions range in size from a few millimeters up to 3–4 cm; not uncommonly, these lesions coalesce into dominant masses as large as 8 cm that distort the renal contour.
The radiologic appearance of malacoplakia reflects the extent of disease and depends on the degree of residual renal capacity. Larger lesions that have replaced and expanded the kidney may compromise the filtering and concentrating functions of the kidney. Subsequently, the lesions tend to minimally enhance at CT and stand out against the vascular blush of the normal renal cortex. The classic appearance is an enlarged kidney with multiple hypovascular masses (Fig 29) (51). Multifocality has been observed in approximately 75% of cases, with bilateral involvement observed in approximately half of these cases (55).
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Figure 29a. Malacoplakia. (a, b) Unenhanced CT images obtained at different levels (a higher than b) demonstrate symmetrically enlarged kidneys. (c) Corresponding T1-weighted MR image shows globally enlarged kidneys of intermediate signal intensity. (d) Photograph of the bisected specimen reveals a whitish infiltrate that nearly completely replaces the renal parenchyma. Scale is in centimeters. (e) Photomicrograph (original magnification, x400; von Kossa calcium stain) shows calcium deposition in a number of cells (Michaelis-Gutmann bodies), a finding that is characteristic of renal malacoplakia. (Reprinted, with permission, from reference 9.)
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Figure 29b. Malacoplakia. (a, b) Unenhanced CT images obtained at different levels (a higher than b) demonstrate symmetrically enlarged kidneys. (c) Corresponding T1-weighted MR image shows globally enlarged kidneys of intermediate signal intensity. (d) Photograph of the bisected specimen reveals a whitish infiltrate that nearly completely replaces the renal parenchyma. Scale is in centimeters. (e) Photomicrograph (original magnification, x400; von Kossa calcium stain) shows calcium deposition in a number of cells (Michaelis-Gutmann bodies), a finding that is characteristic of renal malacoplakia. (Reprinted, with permission, from reference 9.)
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Figure 29c. Malacoplakia. (a, b) Unenhanced CT images obtained at different levels (a higher than b) demonstrate symmetrically enlarged kidneys. (c) Corresponding T1-weighted MR image shows globally enlarged kidneys of intermediate signal intensity. (d) Photograph of the bisected specimen reveals a whitish infiltrate that nearly completely replaces the renal parenchyma. Scale is in centimeters. (e) Photomicrograph (original magnification, x400; von Kossa calcium stain) shows calcium deposition in a number of cells (Michaelis-Gutmann bodies), a finding that is characteristic of renal malacoplakia. (Reprinted, with permission, from reference 9.)
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Figure 29d. Malacoplakia. (a, b) Unenhanced CT images obtained at different levels (a higher than b) demonstrate symmetrically enlarged kidneys. (c) Corresponding T1-weighted MR image shows globally enlarged kidneys of intermediate signal intensity. (d) Photograph of the bisected specimen reveals a whitish infiltrate that nearly completely replaces the renal parenchyma. Scale is in centimeters. (e) Photomicrograph (original magnification, x400; von Kossa calcium stain) shows calcium deposition in a number of cells (Michaelis-Gutmann bodies), a finding that is characteristic of renal malacoplakia. (Reprinted, with permission, from reference 9.)
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Figure 29e. Malacoplakia. (a, b) Unenhanced CT images obtained at different levels (a higher than b) demonstrate symmetrically enlarged kidneys. (c) Corresponding T1-weighted MR image shows globally enlarged kidneys of intermediate signal intensity. (d) Photograph of the bisected specimen reveals a whitish infiltrate that nearly completely replaces the renal parenchyma. Scale is in centimeters. (e) Photomicrograph (original magnification, x400; von Kossa calcium stain) shows calcium deposition in a number of cells (Michaelis-Gutmann bodies), a finding that is characteristic of renal malacoplakia. (Reprinted, with permission, from reference 9.)
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At US, malacoplakia lesions are typically described as poorly defined, hypoehoic masses seen within an enlarged, deformed kidney with distortion of the central echo complex (54).
More recent reports of MR imaging of malacoplakia lesions have described a relatively specific pattern of multiple 1–2-cm nodules with low signal intensity on T1- and T2-weighted images and delayed enhancement of intervening fibrous stroma (56).
In a single case report in which positron emission tomography was performed, intense accumulation of fluorine 18 fluordeoxyglucose was noted (57).
In the appropriate clinical setting, imaging findings can suggest the correct diagnosis. Biopsy is required for confirmation, but this procedure obviates further surgery in most cases, since medical therapy alone has been reported to be more than 90% effective (58).
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Acknowledgments
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The authors acknowledge the contribution of the American Registry of Pathology for many of the histologic images and thank Greg Hall, MD, for assistance with image selection and cropping and Anika Torruella for graphics and word-processing assistance.
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Footnotes
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The opinions or assertions contained herein are the private views of the authors and are not to be construed as official nor as reflecting the views of the Departments of the Army, Navy, or Defense.
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References
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Abstract
LEARNING OBJECTIVES
