An Approach to the Diagnosis of Bladder Lesions in Biopsy and Transurethral Resection Specimens
Section 6 -
Mimics of Urothelial Carcinoma
Mahul B. Amin, MD
Jesse K. McKenney, MD
82-year-old man with urinary obstructive symptoms.
Cystoscopy revealed a 1.5 cm nodular mass at the bladder base.
68-year-old man with urinary obstructive symptoms.
He underwent a TURP and, intraoperatively, a 1.3 cm nodular
lesion was identified in the trigone of the bladder.
Mimics of Urothelial Carcinoma
Mimics of Urothelial Carcinoma
- Papillary/Polypoid cystitis
- Cystitis cystica spectrum
- Nephrogenic adenoma (metaplasia)
- Eosinophilic cystitis
- Treatment related changes
- Pseudocarcinomatous hyperplasia
- Radiation cystitis
- Ectopic prostate
- Paraganglioma (Pheochromocytoma)
- Prostatic adenocarcinoma
- Colonic adenocarcinoma (direct extension)
- Other hematologic malignancies
- Metastatic carcinoma
There are many urothelial and non-urothelial lesions in the urinary bladder that may closely mimic
urothelial carcinoma, both clinically and histologically. The list of mimics outlined in this section is
not exhaustive, but covers the most common lesions encountered on transurethral biopsy.
I. Pseudotumors of the Urinary Bladder that Mimic Carcinoma
1) Papillary/Polypoid cystitis
Papillary/polypoid cystitis is a clinically benign pattern of
urothelial injury usually secondary to an indwelling catheter or a vesical fistula. The papillary and
polypoid patterns may be intermixed, but lesions with relatively slender, non-branching exophytic
projections are termed papillary cystitis, while broad-based, bulbous lesions have been termed polypoid
cystitis. Characteristically, the exophytic appearance results from edema in the lamina propria, but
variable fibrosis, chronic inflammation, and associated dilated blood vessels are also present. These
lesions exist along a morphologic continuum with bullous cystitis depending on the degree of edema. Some
authors have used the following convention: lesions that are taller than they are wide are termed
papillary/polypoid cystitis, and vice versa for bullous cystitis. Older lesions tend to have less edema
with more stromal fibrosis.
The main diagnostic consideration is a papillary urothelial neoplasm, particularly
urothelial papilloma. Small, superficial biopsies of papillary cystitis that do not include the
underlying lamina propria may be histologically indistinguishable from a papilloma because both lesions
typically share a urothelial lining of normal thickness and morphology. In some cases, usually with
recent catheterization, papillary/polypoid cystitis shows marked reactive epithelial changes with small,
prominent nucleoli, urothelial hyperplasia, and mitotic activity. In general, papillomas have more
slender papillae. The papillae of papillary cystitis often have a bulbous tip with prominent stromal
edema. In additon, urothelial papillomas have a few unique features that may aid in the distinction when
a very prominent umbrella cell layer with a hobnail pattern or marked
cytoplasmic vacuolization, a gland-in-gland pattern within the papillae, a dilated lymphatic space
filling the papillae, a more complex papillary pattern with secondary and tertiary branching, and a mixed
endophytic (inverted) component.
2) von Brunn nests/Cystitis cystica/Cystitis cystica glandularis
von Brunn nests represent a normal variation of bladder
histology (most commonly in the trigone) that may result from a prior inflammatory insult. They are
characterized by well-circumscribed, evenly spaced nests of invaginated urothelium in the lamina
propria. In the bladder, the nests typically have smooth, rounded contours and are often clustered in
groups, but the connection with the overlying urothelium may not be identifiable. They are usually
located in the superficial lamina propria, but deeper nests have been described. In the ureter and renal
pelvis, the individual nests are smaller and may have a more irregular contour; however, they maintain a
linear or lobular architecture and have a sharp, linear border at the deep aspect. 
The term cystitis cystica is used when the nests are cystically
dilated with an inner luminal surface. When the inner adluminal cells have a columnar or cuboidal
appearance with prominent apical cytoplasm (not intestinal type goblet cells), the term cystitis cystica glandularis is used. Finally, the presence of intestinal-type
goblet cells within the nests warrants the designation cystitis cystica glandularis
with intestinal metaplasia. Although rare case reports have described adenocarcinoma adjacent to
cystitis cystica glandularis, cystitis cystica is relatively common and is not currently regarded as a
precursor to vesical carcinoma. 
The main differential diagnosis is a "deceptively benign" form of urothelial carcinoma
such as the nested variant.  This distinction is discussed in detail in that section of the
syllabus (variants of urothelial carcinoma: "deceptively bland patterns"). Occasionally, urothelial
carcinoma in-situ may extend into von Brunn nests and mimic invasion. The relatively smooth, round
contour of the nests, the absence of surrounding retraction spaces, the lobular or linear arrangement of
the nests with a non-infiltrative base, and the absence of a stromal reaction should aid in that
distinction. In some instances, the distinction from inverted papilloma (cystitis cystica-like pattern)
may be somewhat arbitrary. Inverted papillomas typically show a more anastomosing pattern of the
epithelial nests and retain the peripheral palisading of cells even when central lumina are present.
Rare examples of florid cystitis cystica with extensive intestinal metaplasia and mucin extravasation
have also been reported.
These florid metaplasias may closely mimic invasive
adenocarcinoma because they fill the lamina propria and abut the muscularis propria. Adenocarcinomas
typically show greater nuclear atypia, more extensive mucin extravasation, and more mitotic activity. In
addition, adenocarcinomas usually present with obvious, destructive invasion of the muscularis propria.
One series of florid cystitis cystica glandularis with intestinal metaplasia reported two cases with
"focal, superficial extension" into the muscularis propria,  but this likely represents an
irregular muscularis/lamina propria junction and is distinctive from the extensive, irregular invasion of
the muscularis propria.
3) Nephrogenic adenoma (metaplasia)
Nephrogenic adenoma is a benign proliferative lesion occurring
in the bladder (80%), urethra (12%), or ureters (8%) that is thought to arise secondary to urothelial
injury. These lesions are usually small (less than 1 cm), but have been reported to reach sizes as large
as 7 cm. 19 % of patients with nephrogenic adenoma have multiple lesions. The main importance of
recognizing this lesion is its distinction from papillary urothelial bladder neoplasms and prostatic
adenocarcinoma. Although a broad histologic spectrum has been reported for nephrogenic adenoma, there
are three main growth patterns that are often intermixed, and will be discussed separately:
papillary/polypoid, tubular, and diffuse.  The individual cells also have a variable
morphology; they are typically low cuboidal with scant eosinophilic cytoplasm. They frequently have
prominent nucleoli, but, by definition, nephrogenic adenomas do not show marked nuclear atypia (irregular
nuclear membranes, irregular chromatin condensation, nuclear pleomorphism) or easily identified mitotic
activity. Degenerative type atypia has been described, however, and is characterized by large cells with
a hyperchromatic appearance secondary to a smudged, indistinct chromatin pattern (similar to so-called
"ancient change" in Schwannomas). Other rare features of nephrogenic adenoma include cytoplasmic
clearing or bulbous apical nuclei producing a hobnail pattern.
The tubular pattern is most common and consists of well-delineated tubules lined by a
single layer of low columnar to cuboidal epithelium occasionally with prominent nucleoli. Most
frequently, the individual tubules are well-spaced with intervening stroma, but the tubules may be very
compact (back-to-back), imparting a solid, nested appearance focally. The tubules may also become
dilated imparting a cystic appearance. In these cystic patterns, the epithelial lining is frequently
flattened and attenuated. There is also variable peritubular hyalinization with a basement membrane-like
appearance, and intraluminal eosinophilic and basophilic secretions are relatively common. Small
compressed tubules with only a single lining cell apparent at the periphery of the lumen may closely
resemble a signet-ring cell, but this is usually present only focally. The degenerative appearing cells
described above typically line tubules that are flattened and can resemble blood vessels.
The papillary/polypoid pattern of nephrogenic adenoma is most commonly characterized by large
edematous polypoid excrescenses, but a relatively simple, filiform branching pattern is also seen in a
minority of cases (approximately 10%). Complex epithelial budding is rare, and usually focal. The
polypoid excresences and papillae are lined by a single layer of low cuboidal cells with scant
eosinophilic cytoplasm. The cytoplasm is occasionally more prominent with an oncocytic appearance or
more cuboidal with pale cytoplasm.
The "diffuse" pattern is rare, and is almost always admixed with other patterns of nephrogenic
adenoma. It is characterized by a very compact or solid growth pattern with little to no intervening
stroma. A cord-like growth pattern somewhat reminiscent of a carcinoid tumor has also been reported in
these diffuse areas.
Nephrogenic adenoma typically has a laminar distribution underlying the urothelium with a sharp line
of demarcation within the lamina propria at the base. Although it seems infrequent, there are rare
reports of extension into the superficial muscularis propria and into prostatic stroma. We
would recommend extreme caution in making the diagnosis of nephrogenic adenoma with muscularis propria
involvement; a "deceptively bland" pattern (tubulocystic pattern) of urothelial carcinoma should be
carefully considered in that setting. That distinction is discussed in detail in the variants portion of
the syllabus (variants of urothelial carcinoma: "deceptively bland patterns").
The main differential diagnostic consideration for the tubular pattern is prostatic
adenocarcinoma. The well-spaced architectural arrangement of the tubules, the peritubular hyalinization,
epithelial flattening with cystic change, and mixed papillary/polypoid patterns should aid in the
diagnosis of nephrogenic adenoma. Immunohistochemistry may be misleading in this setting because weak
cytoplasmic immunoreactivity with PSA or PSAP is reported in nephrogenic adenoma. In addition, P504S
(alpha-methylacyl-CoA racemase) immunoreactivity has also recently been documented in nephrogenic adenoma
and should, therefore, not be used as a distinguishing marker for prostatic adenocarcinoma in this
The main differential diagnosis for papillary/polypoid nephrogenic adenoma is a low-grade papillary
urothelial neoplasm (papilloma, PUNLMP, or low grade carcinoma). In general, papillary urothelial
neoplasms have a stratified lining consisting of multiple cell layers. In addition, the individual
neoplastic cells of urothelial tumors have more elongated cells, often with nuclear grooves.
Higher-grade urothelial carcinomas have nuclear pleomorphism, nuclear hyperchromasia, and increased
mitotic activity, making their distinction somewhat more straightforward. Identification of a mixed
tubular pattern in a nephrogenic adenoma may also be helpful in this differential diagnostic setting.
The diagnosis of clear cell adenocarcinoma of the bladder is often considered in this setting because
of the mixed papillary/ tubulo-cystic pattern. Clear cell carcinomas, however, typically have marked
nuclear pleomorphism, obviously increased mitotic activity, more cellular stratification, and more
prominent cytoplasmic clearing. Some authors have suggested the utility of p53 stains in this
differential setting (nuclear reactivity in adenocarcinoma), but most authors use the
morphologic features discussed above.
A recent study has reported the potential utility of immunohistochemistry for PAX2 in this
differential diagnostic setting. Nuclear reactivity for PAX2 in nephrogenic adenoma may aid in the
distinction from prostatic adenocarcinoma. [84 ]Its utility in the distinction from other
lesions such as clear cell carcinoma requires further study.
Endometriosis may involve the bladder and is morphologically
identical to that seen in other, more common anatomic locations.
The diagnosis rests on
the identification of cytologically bland endometrial-type glands surrounded by a cuff of endometrial
stroma that is characterized by small, cytologically bland round to fusiform cells with little cytoplasm.
Curiously, there are case reports of vesical endometriosis occurring in men, possibly related to
The presence of endocervical, tubal, and endometrial type glands (without associated stroma) within
the wall of the bladder has also been described.
They are usually present within the
muscularis propria, but may extend to the perivesical soft tissue or the lamina propria. The glands are
typically haphazardly arranged within the smooth muscle of the posterior wall or posterior dome, and are
commonly lined by columnar, endocervical type epithelium with no significant cytologic atypia (no
pleomorphism, hyperchromasia, or increased mitotic activity). The individual glands may be rounded or
irregularly shaped, and cystic dilation is common. The reported series describe adjacent stroma with no
response or a surrounding fibrous stroma that is focally loose and edematous with admixed acute and
chronic inflammatory cells. Mucin extravasation secondary to gland rupture is common in these lesions
and typically elicits a reactive fibroblastic or histiocytic response. The diagnostic term endocervicosis has been used when the glands are composed of purely endocervical
with the term müllerianosis reserved for mixed
The differential diagnosis with primary vesical adenocarcinoma and urachal
carcinoma is discussed in those sections of the syllabus (variants of urothelial carcinoma:
6) Eosinophilic cystitis
" Eosinophilic cystitis" is a descriptive term that has been
applied to mixed inflammatory infiltrates of the lamina propria rich in eosinophils. It is best regarded
as a pattern of inflammation associated with a variety of causes and not a single diagnostic entity.
Clinically, it often has a polypoid appearance mimicking polypoid cystitis or urothelial carcinoma in
adults, and rhabdomyosarcoma in children. In children, bladder eosinophilia has been reported in
association with allergic gastroenteritis, asthma, or other allergic disorders.
adults, it is more frequently associated with prostatic hyperplasia, bladder carcinoma, or prior biopsy.
Rarely, it may be secondary to a parasitic infection. 
Malakoplakia is an inflammatory lesion that is caused by
impaired intraphagosomal digestion resulting in histiocytic accumulation.  It occurs in a
variety of anatomic locations, but is most common in the urinary bladder and typically associated with a
coliform bacterial infection (often E. coli). Morphologically, it consists
of sheets of histiocytes with granular eosinophilic cytoplasm (von Hansemann cells) with small basophilic
intracytoplasmic inclusions (Michaelis-Gutmann bodies). The histiocytes are typically in the lamina
propria with an intact, overlying urothelium. The inclusions are spherical, concentrically laminated
(imparting a "bull's eye" appearance), and typically range from 5-8 microns in size. The inclusions
contain calcium, so they are highlighted by von Kossa stain.
The main differential diagnostic consideration is urothelial carcinoma with a sheet-like
growth pattern. The small bland nuclei of the histiocytes and identification of the Michaelis-Gutman
bodies are usually sufficient for this distinction. In more difficult cases, an absence of cytokeratin
immunoreactivity may be helpful.
8) Pseudocarcinomatous hyperplasia associated with radiation or chemotherapy
Rarely, patients with radiation or chemotherapy cystitis
present with an unusual, benign epithelial proliferation on biopsy that can closely mimic invasive
istologically, these epithelial proliferations are within the
lamina propria (they do not involve muscularis propria) and consist of small nests of urothelium with
variable rounded to irregular, jagged contours creating an infiltrative appearance. The individual
urothelial cells may have a "squamoid" appearance and show some nuclear enlargement with slight variation
in nuclear size, but the nuclear chromatin is bland and they do not show the degree of atypia (marked
pleomorphism and hyperchromasia) required for a diagnosis of carcinoma in situ or high grade urothelial
carcinoma. The most helpful and unique feature of these lesions is that the epithelial nests wrap around
blood vessels with associated fibrin and congestion. The fibrin is found both within the wall of the
vessels and within the lamina propria. Associated hemorrhage, fibrosis, acute and chronic inflammation,
and ulceration are also common, as well as other, radiation-induced changes such as ectatic vessels with
The main differential diagnostic consideration is an invasive urothelial carcinoma. In
the pseudocarcinomatous proliferations, the lack of significant nuclear atypia, the presence of other
radiation-induced changes, and, most importantly, the intimate association of the epithelium with blood
vessels and fibrin generally allow this distinction.
9) Radiation cystitis
Radiation cystitis typically mimics urothelial carcinoma
in-situ, both clinically and histologically. It is, therefore, discussed in that section of the
The bladder can be involved by systemic amyloidosis or,
rarely, by primary amyloidosis. The morphologic appearance is identical to that seen in other anatomic
sites: deposits of an eosinophilic, amorphous material. The amyloid is typically present in the lamina
propria with extension into deeper connective tissue. Perivascular amyloid deposits are, reportedly,
less common. As in other locations, Congo red stains are typically used for confirmation.
11) Ectopic prostate tissue 
Ectopic prostate tissue presenting as a polypoid mass lesion
in the bladder (usually the trigone) has been reported. The morphologic appearance is identical to that
described for benign prostatic urethral polyps. The submucosal component consists of admixed stroma and
histologically benign prostate glands. The overlying surface is often papillary with a lining consisting
of prostatic epithelium, urothelium, or an admixture of both. Identification of the prostatic epithelial
component usually allows distinction from a papillary urothelial neoplasm.
Neoplasms Involving/or Primary to the Urinary Bladder that Mimic Urothelial Carcinoma
1) Paraganglioma (Pheochromocytoma)
Paragangliomas (pheochromocytoma) may occur in the bladder and
closely mimic urothelial carcinoma. Clinically, patients are usually somewhat younger (median- 44 years)
than those with urothelial carcinoma. Presentation with symptoms related to hormone release (urinary
urgency, headache, anxiety, and sweating) have been reported, but in the most recently reported series
these symptoms only present in 19% of cases.
Histologically, as in carotid body tumors, paragangliomas characteristically grow in a
nested or "zellballen" pattern with an associated delicate fibrovascular stroma. In some cases, the
nests of neoplastic cells are less tightly clustered because of marked stromal fibrosis making the
zellballen pattern less recognizable, a pattern similar to paragangliomas of the middle ear. A minority
of cases show a diffuse sheet-like growth pattern, but a nested pattern can usually be identified
focally. The neoplastic cells usually have abundant amphophilic or eosinophilic cytoplasm, sometimes
with a slightly granular appearance. The nuclei typically are round with smooth contours, even
chromatin, small nucleoli, and occasional nuclear inclusions. Scattered pleomorphic cells with smudged,
hyperchromatic nuclei are occasionally found as seen in other endocrine tumors (i.e. "endocrine
anaplasia"), and rare cases show nuclear clearing. Paragangliomas may be present anywhere within the
bladder wall (including the muscularis propria), but no surrounding stromal reaction is present.
Although many reported cases of paraganglioma in the urinary bladder have followed a benign clinical
course, late metastases are known to occur. As in other anatomic sites, it has been difficult to
establish histologic criteria to definitively predict behavior, and long-term follow-up care is
The main differential is an invasive urothelial carcinoma, however, the characteristic
nested pattern with fibrovascular septa, the usually bland cytology, the absence of a stromal reaction,
and the absence of appreciable mitotic activity should suggest the diagnosis of paraganglioma.
Immunohistochemistry is usually confirmatory, as paragangliomas are reactive for neuroendocrine markers
(chromogranin and synaptophysin) and non-reactive for cytokeratin, while the opposite is true of
The possibility of a carcinoid tumor may also be considered, but the absence of even focal
cytokeratin expression should exclude that possibility. Melanoma might show some morphologic overlap,
but paragangliomas have a distinctive s-100 protein reactivity pattern (expression in sustentacular cells
surrounding the nests) and are non-reactive for other, more specific melanoma markers (HMB-45 and
2) Prostatic adenocarcinoma
Prostatic adenocarcinoma may present clinically as a bladder
mass at cystoscopy. Characteristic features of prostatic adenocarcinoma that aid in the distinction from
urothelial carcinoma include the usual monotonous appearance of the nuclei, sometimes prominent nucleoli,
and focal acinar differentiation. Recent reports highlight rare prostatic adenocarcinomas with nuclear
anaplasia that may closely mimic urothelial carcinoma.
Cases with a sheet-like growth
pattern or more nuclear pleomorphism may require immunohistochemical studies. Prostatic adenocarcinoma
is typically immunoreactive for PSA and PSAP, but negative for high molecular weight cytokeratin, and the
opposite immunophenotype is typical of urothelial carcinoma. One large study has recommended PSA, PSAP,
and cytokeratin 34BE12 as an initial panel with Leu7, cytokeratin 7, and p53 as a secondary
panel.  The utility of uroplakin III and thrombomodulin as markers of urothelial
differentiation has also been proposed,  and one study has demonstrated their utility in
this diagnostic setting.  Lastly, p63 expression is reported in most urothelial carcinomas
and is less frequently expressed in prostatic carcinoma. 
The reported immunoprofiles are summarized below.
Prostatic vs. Urothelial Carcinoma: Immunoprofiles
| ||Prostate ||Urothelial|
|PSA ||68-94% ||0%|
|PSAP ||78-95% ||0%|
|HMWCK (34ßE12) ||6-10% ||65-100%|
|Uroplakin III ||0% ||57-60%|
|Thrombomodulin ||0% ||49-69%|
|p63 ||0-18% ||70-75%|
|CD57 (Leu 7) ||94% ||17%|
PSA: Prostate-specific antigen; PSAP: Prostate-specific acid phosphatase; HWWCK: High-molecular
3) Colonic adenocarcinoma (direct extension)
Colonic adenocarcinoma may involve the bladder by direct
extension and present as an intravesical mass for biopsy. The morphology is typical of colonic
adenocarcinoma, but may be morphologically indistinguishable from a primary bladder adenocarcinoma. This
differential diagnosis is discussed fully in the section on primary adenocarcinoma of the bladder (See
Variants of Urothelial Carcinoma).
Primary malignant melanoma of the genitourinary tract is most
common in the urethra, but has been reported in the bladder as well. These neoplasms have similar
morphologies to those occurring in the skin with a broad morphologic spectrum. Immunostains for s-100
protein, HMB-45, and Melan A are useful for confirmation. As with all diagnoses of melanoma, the
possibility of metastasis from a cutaneous primary must be excluded clinically before the tumor is
accepted as vesical primary.
5) Plasmacytoma/Multiple myeloma 
Rare plasma cell neoplasms may involve the bladder as primary
tumors or, more commonly, as secondary involvement in patients with myeloma. These neoplasms may closely
mimic the plasmacytoid variant of urothelial carcinoma, but immunostains for cytokeratin are usually
sufficient for this distinction. One should be cautious in the use of the CD138 antibody for plasma
cells, because reactivity in carcinomas is well documented. 
6) Other hematologic malignancies
An in depth discussion of lymphoma is beyond the scope of this course, but almost all
types of hematologic malignancy have been reported to involve the bladder secondarily. The most common
primary vesical lymphoma is extranodal marginal zone lymphoma (MALT-type lymphoma). 
Most diagnostic difficulties arise in the setting of a high-grade undifferentiated
neoplasm with cellular discohesion in which both carcinoma and high-grade lymphoma such as diffuse large
B-cell lymphoma are considered. Immunostains for both epithelial and lymphoid markers usually allow
distinction in this setting.
7) Metastatic carcinoma
There are case reports of metastatic carcinomas involving the
bladder from many different anatomic sites. The most common tumors that involve the urinary bladder
secondarily (local extension or metastasis) have been discussed elsewhere in relevant sections of the
course where their morphologies overlap considerably with primary bladder tumors.
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Pseudocarcinomatous hyperplasia associated with radiation therapy
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Ectopic prostate tissue
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Colonic adenocarcinoma (direct extension)
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