DOI:10.2214/AJR.06.0920
AJR 2007; 188:1380-1387
© American Roentgen Ray Society
Renal Pseudotumors
Shweta Bhatt1,
Gregory MacLennan2 and
Vikram Dogra1
1 Department of Radiology, University of Rochester School of Medicine and
Dentistry, 601 Elmwood Ave., Box 648, Rochester, NY 14642.
2 Department of Pathology, Case Western Reserve University, Cleveland, OH.
Received July 24, 2006;
accepted after revision October 11, 2006.
Address correspondence to V. Dogra
(vikram_dogra{at}urmc.rochester.edu).
Abstract
OBJECTIVE. Renal cell carcinoma is the most common malignant tumor
to involve the kidneys; however, a number of other entities—called renal
pseudotumors—may mimic renal neoplasms on imaging. This article presents
the imaging features and pathologic correlation of some of the common and
uncommon renal pseudomasses.
CONCLUSION. Many renal lesions look similar to renal cell carcinoma
on radiologic imaging. The imaging features of renal pseudotumors presented in
this article will help radiologists to identify them and to triage these
patients for appropriate management.
Keywords: genitourinary imaging • kidney disease • renal disease
Introduction
Renal neoplasm is a common occurrence that is easily diagnosed using
routine imaging. However, less is known about the lesions that mimic a renal
neoplasm on imaging yet are proven at subsequent surgery and histopathology to
be a wrong radiologic diagnosis. Such masses may be composed of normal or
benign renal tissue and are referred to as renal pseudotumors. "Although
common lesions such as abscesses and renal cysts may be confidently diagnosed
on imaging, atypical presentations of such common entities and certain
uncommon entities may simulate renal neoplasms and may lead to an unnecessary
resection because of the concern for renal malignancy"
[1].
This article presents the imaging features and pathologic correlation of
some of the common and uncommon renal pseudomasses such as splenorenal fusion,
renal pelvic hematomas, xanthogranulomatous pyelonephritis, extramedullary
renal hematopoiesis, and arteriovenous malformation.
Renal pseudotumors may be categorized as developmental, infectious,
granulomatous, and vascular in nature
(Appendix 1).
APPENDIX 1 : Types of Renal Pseudotumors
| Developmental |
| Prominent columns (septa) of Bertin |
| Persistent fetal lobulation |
| Dromedary hump |
| Splenorenal fusion |
| Cross-fused renal ectopia |
| Infectious |
| Abscess |
| Pyelonephritis |
| Scarred kidney |
| Granulomatous |
| Xanthogranulomatous pyelonephritis |
| Sarcoidosis |
| Malakoplakia |
| Tuberculosis |
| Vascular |
| Extramedullary hematopoiesis |
| Arteriovenous malformation |
| Renal pelvic hematomas |
| Anticoagulant-induced subcapsular hemorrhage |
| Miscellaneous |
| Regenerating nodule after reflux |
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Developmental Renal Pseudotumors
Prominent Columns of Bertin
Prominent (or hypertrophied) columns of Bertin (also known as "septa
of Bertin") is a normal variant of the kidney formed of hyper-trophied
cortical tissue located between the pyramids that projects into the renal
sinus, resulting in splaying of the sinus. Hypertrophied but otherwise normal
renal tissue not only distorts the renal sinus but can also result in what
appear to be bizarre or disorganized calyces on excretory urography or CT
urography because the papillae are not situated in the typical radial
orientation. Columns of Bertin is usually located in the middle third of the
kidney, more commonly the left kidney than the right
[2]. Unusually large or
atypical presentation of the prominent columns (septa) of Bertin on sonography
may lead to further imaging, such as CT or MRI of the kidneys, to rule out an
intrarenal tumor (Fig. 1A,
1B,
1C). Some sonographic features
described in the literature that are suggestive of, but not specific for, a
prominent columns (septa) of Bertin include "indentation on the renal
sinus by the lesion, splitting of the sinus, well defined and distinct from
the renal sinus, in continuity with the adjacent renal cortex, with similar
echogenicity as that of adjacent renal cortex, engulfment of the papilla, and
a cortical projection due to extension of the junctional parenchyma medially
in the kidney" [3].
Although most people believe that the columns of Bertin has similar
echogenicity to the adjacent renal cortex, according to Yeh et al.
[4] a true columns of Bertin
appears more echogenic than the normal renal cortex as a result of the
anisotropic effect [5]. Because
of the nonspecific nature of the previously described sonographic findings,
patients with an atypical sonographic appearance or unusually large and
prominent columns (septa) of Bertin are usually followed up with
contrast-enhanced CT or MRI. Prominent columns (septa) of Bertin can be
confirmed by showing its enhancement (perfusion) to be similar to that of
surrounding renal parenchyma on contrast-enhanced CT, MRI, or
contrast-enhanced sonography.
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Fig. 1A —46-year-old man with hypertrophied columns (septa) of Bertin.
(Reprinted with permission from Paspulati RM, Bhatt S. Sonography in benign
and malignant renal masses. Ultrasound Clinics 2006; 1:25-41
[2]) Longitudinal gray-scale
sonogram of left kidney shows large hypertrophied columns of Bertin
(arrows) located in middle third of kidney. It is continuous with
normal renal cortex, and smooth renal surface overlies this pseudotumor.
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Fig. 1B —46-year-old man with hypertrophied columns (septa) of Bertin.
(Reprinted with permission from Paspulati RM, Bhatt S. Sonography in benign
and malignant renal masses. Ultrasound Clinics 2006; 1:25-41
[2]) Follow-up MRI was
performed to rule out renal tumor. T1-weighted fat saturated (B) and
gadolinium-enhanced (C) images of kidneys confirm presence of
hypertrophied columns of Bertin (arrows), which shows similar signal
intensity and identical homogeneous enhancement as that of normal renal
cortex.
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Fig. 1C —46-year-old man with hypertrophied columns (septa) of Bertin.
(Reprinted with permission from Paspulati RM, Bhatt S. Sonography in benign
and malignant renal masses. Ultrasound Clinics 2006; 1:25-41
[2]) Follow-up MRI was
performed to rule out renal tumor. T1-weighted fat saturated (B) and
gadolinium-enhanced (C) images of kidneys confirm presence of
hypertrophied columns of Bertin (arrows), which shows similar signal
intensity and identical homogeneous enhancement as that of normal renal
cortex.
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Dromedary Hump
Dromedary hump appears as a focal bulge on the lateral border of the left
kidney (Fig. 2). It forms as a
result of the adaptation of the kidney to the adjacent spleen. It can usually
be easily diagnosed on sonography and has the same perfusion as the
surrounding renal parenchyma on contrast-enhanced sonography
[6].
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Fig. 2 —25-year-old man with dromedary hump. Longitudinal gray-scale
sonogram of left kidney shows presence of focal bulge (arrow) on
lateral border of left kidney that has similar echotexture as adjacent renal
cortex. Adjacent spleen (SP) is visualized, which is causing impression on
kidney. (Reprinted with permission from Paspulati RM, Bhatt S. Sonography in
benign and malignant renal masses. Ultrasound Clinics 2006; 1:25-41
[2])
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Persistent Fetal Lobulation (Lobation)
The fetal kidneys are subdivided into lobes that may be separated by
grooves. This lobulation usually diminishes by the end of the fetal period.
Sometimes these lobulations persist into adulthood, and if not correctly
identified, may be misdiagnosed as a renal tumor or a scarred kidney.
Lobulation is characterized on sonography by the presence of renal surface
indentations that overlie the space between the pyramids
(Fig. 3), as compared with true
renal scars, which are located overlying the medullary pyramids.
Radiologically, persistent fetal lobulation of the kidney can be confirmed by
documenting the presence of a renal pyramid in the bulge bounded by septa of
Bertin on either side [3].
Scars related to renal infarcts are typically situated between pyramids.
However, their focal nature usually allows them to be differentiated from
fetal lobulations.
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Fig. 3 —32-year-old man with persistent fetal lobulation. Longitudinal
gray-scale sonogram of right kidney shows sharp indentation (arrow)
overlying space between pyramids. Resultant focal bulge on renal surface
mimics renal tumor and should be carefully scanned to confirm presence of
normal renal tissue within it.
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Splenorenal Fusion
Splenorenal fusion is a rare benign entity; to our knowledge, only six
cases of developmental splenorenal fusion have been described in the
literature. Splenorenal fusion refers to the presence of heterotopic splenic
tissue in the renal capsule. It may arise as a developmental anomaly secondary
to the fusion of nephrogenic mesoderm and splenic anlage in the second month
of gestation [7]. It may also
be secondarily acquired as a result of splenosis after trauma or splenectomy,
and the presence of a renal mass in such patients should raise the suspicion
of splenosis.
Splenorenal fusion usually involves the left kidney, but its presence on
the right side has also been documented. Patients usually present with an
asymptomatic mass or, rarely, with symptoms of hypersplenism (anemia). On CT
or gadolinium-enhanced MRI, splenorenal fusion appears as a solid enhancing
mass arising from the kidney (Figs.
4A,
4B,
4C and
4D); a 99mTc sulfur
colloid scan is confirmatory and shows uptake by the splenic tissue.
Fine-needle aspiration biopsy or ferumoxides-enhanced MRI
[8] may also be useful to
confirm the diagnosis. Pathologically, the lesion consists of
hemorrhagic-appearing tissue in the renal capsule, but it is distinctly
separate from the adjacent normal renal parenchyma
[1]
(Fig. 4E).
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Fig. 4A —53-year-old woman with splenorenal fusion. Axial T1-weighted
(A) and coronal T2-weighted (B) MRI images of kidneys show
well-defined mass (arrow) in lower pole of left kidney, which is
hypointense on T1-weighted and has intermediate signal on T2-weighted images.
Multiple renal cysts are also present bilaterally.
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Fig. 4B —53-year-old woman with splenorenal fusion. Axial T1-weighted
(A) and coronal T2-weighted (B) MRI images of kidneys show
well-defined mass (arrow) in lower pole of left kidney, which is
hypointense on T1-weighted and has intermediate signal on T2-weighted images.
Multiple renal cysts are also present bilaterally.
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Fig. 4E —53-year-old woman with splenorenal fusion. Gross specimen of left
kidney after nephrectomy reveals mass consists of hemorrhagic-appearing
splenic tissue (SP) in renal capsule but sharply demarcated from adjacent
renal parenchyma (K), confirming splenorenal fusion. (Reprinted with
permission from Tynski Z, MacLennan GT. Renal pseudotumors. J Urol
2005; 173:600 [1].
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Infectious Renal Pseudotumors
Focal Pyelonephritis
Renal infection confined to a single lobe is called focal pyelonephritis
(Fig. 5). Renal infection
involving multiple lobes of the kidney is referred to as multifocal
pyelonephritis. It is more common in patients with diabetes and those who are
immunocompromised. Patients typically present with flank pain, fever with
chills, and pyuria. Focal pyelonephritis is seen on sonography as either a
hypoechoic or hyperechoic lesion in the renal cortex extending from the renal
medulla to the renal capsule, with decreased perfusion on color-flow Doppler
imaging. CT shows a focal wedge-shaped area of low attenuation without a
well-defined wall around it, and without an overlying bulge on the renal
surface, which distinguishes it from renal cell carcinoma. Striations may also
be observed in the nephrogram. Renal cortical scintigraphy, using
99mTc-labeled glucoheptonate or dimercaptosuccinic acid (DMSA), is
more sensitive and specific for focal pyelonephritis than any other imaging
technique and shows a focal cortical defect in the kidney
[9]. Newer sonography
techniques, such as tissue harmonic imaging, pulse inversion harmonic imaging,
and contrast-enhanced sonography, may also be useful in the early detection of
focal pyelonephritis [10].
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Fig. 5 —35-year-old woman with focal pyelonephritis. Contrast-enhanced CT
scan of kidneys shows focal hypoattenuating lesion (arrowheads) in
right kidney with decreased contrast enhancement. Absence of distinct wall
around lesion and clinical information suggestive of infection are helpful in
distinguishing this lesion from renal tumor.
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Extension of the acute inflammatory process into the perirenal soft tissues
may give the appearance of a renal malignancy. Some infiltrative renal tumors
(particularly medullary renal carcinoma) may have an appearance similar to
that of focal pyelonephritis. In such cases, clinical information can be
helpful in making a diagnosis.
Renal Abscess
Renal abscesses are primarily caused by an ascending infection from the
lower urinary tract with gram-negative bacilli and enteric bacteria, such as
Escherichia coli, Klebsiella species, and Proteus species.
Sonography and CT reveal a well-defined heterogeneous mass (Figs.
6A and
6B) that at times may simulate
a renal malignancy. Features such as irregular walls with increased
through-transmission on sonography and a low-attenuation lesion with enhancing
walls on CT, along with a history of fever and a positive urinalysis and
culture, indicate a renal abscess
[11]. Differentiation from a
renal malignancy may be difficult if clinical information does not support the
presence of infection. Pathologically, renal abscess is identified by the
presence of pus and debris with varying degrees of reactive inflammatory
changes (Fig. 6C).
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Fig. 6B —36-year-old man with left renal abscess. Corresponding
contrast-enhanced CT scan of kidneys shows low-attenuation mass
(arrow) in mid region of left kidney simulating renal cell
carcinoma.
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Scarred Kidney
Severely scarred kidney secondary to infectious processes such as
pyelonephritis or renal infarcts may also present as a potential pseudotumor
on imaging. Regions of preserved parenchyma may appear masslike on sonography
or even in the nephrographic phase of CT and MRI. Appropriate corticomedullary
differentiation in the early phases of enhancement on CT or MRI may be
required to exclude a mass.
Granulomatous Renal Pseudotumors
Xanthogranulomatous Pyelonephritis (XGP)
XGP is a rare inflammatory condition usually secondary to chronic
obstruction caused by nephrolithiasis and resulting in infection and
irreversible destruction of the renal parenchyma. XGP is associated with a
staghorn calculus in approximately 70% of cases. Patients with diabetes are
particularly predisposed to the formation of XGP. XGP may rarely present with
the classic urographic triad of unilaterally decreased or absent renal
excretion, staghorn calculus, and diffuse renal enlargement
[12]. XGP may present in a
diffuse or focal pattern. Focal or segmental XGP is more likely to mimic renal
cell carcinoma on imaging because of its radiologic similarities, which often
result in its resection.
Establishing a definite preoperative diagnosis only on the basis of imaging
in both focal and diffuse forms of XGP is difficult. Sonographically, XGP may
appear as single or multiple hypoechoic areas in the parenchyma of an enlarged
kidney, with central echogenic foci representing calculi. Sonographic findings
are nonspecific but can nevertheless suggest a diagnosis of XGP. Although not
confirmatory, CT evaluation can be considered helpful in the presence of
features such as abscess replacing the renal parenchyma, with low-attenuation
areas (lipid-rich xanthogranu-lomatous tissue) and calcification in the mass
[13] (Figs.
7A and
7B). If calculi are not
present, focal XGP with a low-attenuation area in the renal parenchyma may
suggest a diagnosis of renal tumor. MRI has no advantage over CT and is
usually not performed.
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Fig. 7A —47-year-old woman with xanthogranulomatous pyelonephritis (XGP).
Contrast-enhanced CT scans of kidneys show enlarged right kidney with focal
area of hypodensity (white arrow, A). Also seen is presence of
calculus (arrowhead, B) and part of stent (black
arrow, A) in right renal pelvis.
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Fig. 7B —47-year-old woman with xanthogranulomatous pyelonephritis (XGP).
Contrast-enhanced CT scans of kidneys show enlarged right kidney with focal
area of hypodensity (white arrow, A). Also seen is presence of
calculus (arrowhead, B) and part of stent (black
arrow, A) in right renal pelvis.
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Pathologically, XGP is composed of multiple inflammatory cells, both acute
and chronic, and xanthoma cells, which are lipidladen foamy macrophages that
impart their yellow color to the mass
[1] (Figs.
7C,
7D and
7E).
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Fig. 7C —47-year-old woman with xanthogranulomatous pyelonephritis (XGP).
Surgical specimen of kidney (K in C) shows focal XGP (C) and
necrotic debris (D). Debris was originally in cavity seen in
C.
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Fig. 7D —47-year-old woman with xanthogranulomatous pyelonephritis (XGP).
Surgical specimen of kidney (K in C) shows focal XGP (C) and
necrotic debris (D). Debris was originally in cavity seen in
C.
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Fig. 7E —47-year-old woman with xanthogranulomatous pyelonephritis (XGP).
Microscopic slide shows abundant lipid-laden macrophages
(arrowheads), xanthoma cells, with multiple acute and chronic
inflammatory cells. (H and E, x40) (Reprinted with permission from
Tynski Z, MacLennan GT. Renal pseudotumors. J Urol 2005; 173:600
[1])
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Other Granulomatous Renal Pseudotumors
Sarcoidosis and malakoplakia are other rare granulomatous mass lesions that
mimic a renal malignancy.
Sarcoidosis—Sarcoidosis is a multisystem disorder with
varied extrapulmonary symptoms. In the United States, sarcoidosis is more
common in the African American population, with age-adjusted annual incidence
rates of 35.5 per 100,000 for African Americans and 10.9 per 100,000 for
whites [14].
The disorder is characterized by the presence of noncaseating granulomas in
multiple organs of the body
[15]. Renal sarcoidosis can
present in several ways, most commonly as aberrant calcium metabolism,
including hypercalcemia, hypercalciuria (seen in 15-62% patients)
[16], and nephrocalcinosis.
Granulomatous involvement of the kidney has been reported in 7-22% of patients
with sarcoidosis at autopsy, but radiographically distinct renal granulomas
are rarely seen. Radiographically distinct lesions appear on contrast-enhanced
CT as multiple small (2-3 cm), low-attenuation nodular masses in the renal
parenchyma that simulate renal lymphoma or metastasis. Diffuse granulomatous
infiltration of the kidney is a more rare radiologic finding than multiple
nodules. Differentiation is usually done on the basis of the clinical setting,
such as African American race and sickle cell trait, which favor
sarcoidosis.
Granulomatous involvement of the kidney may also cause interstitial
nephritis, which appears as a striated nephrogram on contrast-enhanced CT
[17]. Biopsy is the only way
to confirm the diagnosis. PET may show increased 18F-FDG uptake by
sarcoidosis, which, along with clinical information and the new radiotracers
such as fluoro-
-methyltyrosine, may be helpful in distinguishing renal
sarcoidosis from malignant disease of the kidney
[18].
Malakoplakia—Malakoplakia of the kidney is a rare
inflammatory disorder related to defective macrophage function and is
characterized by the deposition of soft, yellow-brown plaques in the kidney
[13]. There is usually an
underlying urinary tract infection that results in the formation of plaques in
the bladder and the kidney. Radiologically, malakoplakia may appear as an
enlarged kidney, a low-attenuation mass, or a diffuse infiltrative disease.
Radiologic findings in renal malakoplakia are nonspecific and suggest an
alternate diagnosis such as a renal tumor. Isolated renal malakoplakia without
the presence of concurrent lower urinary tract involvement is rare and is more
likely to be mistaken for a renal malignancy on radiologic studies. Diagnosis
of malakoplakia is confirmed by histology. Microscopically, the presence of
Michaelis-Gutmann bodies is pathognomonic of malakoplakia.
Vascular Renal Pseudotumors
Arteriovenous Malformation (AVM)
AVM may be congenital or acquired, with the most common cause being trauma.
Other causes are surgery, tumors, or idiopathic. Arteriovenous fistulas
comprise 70-80% of AVMs in the kidney
[19]. Renal AVMs may be
intraparenchymal or in the renal sinus
(Fig. 8A), and therefore may
be difficult to distinguish from a renal malignancy such as renal cell
carcinoma or transitional carcinoma on contrast-enhanced CT because both these
lesions will show enhancement. Sonography can exclude the possibility of a
solid mass by showing anechoic spaces in the lesion that fill with color on
color-flow Doppler sonography. A mass can be confirmed to be an AVM when a
typical arteriovenous flow pattern is depicted in the lesion (Figs.
8B and
8C). MRI can also be useful in
differentiating an AVM from a malignancy by showing internal flow voids in the
lesion. Gadolinium-enhanced MRI can confirm an AVM during early arterial phase
imaging, where it reveals the presence of abnormal tortuous vessels and an
early draining vein characteristic of an AVM.
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Fig. 8A —35-year-old man with renal arteriovenous malformation. Nephrographic
phase of contrast-enhanced CT scan of kidneys in this patient with no history
of trauma or biopsy shows enhancing lesion in renal pelvis
(arrowheads).
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Fig. 8B —35-year-old man with renal arteriovenous malformation. Subsequent
gray-scale (B) and color Doppler (C) sonograms reveal anechoic
structures (arrows, B) in renal pelvis (excluding possibility
of solid mass), which fill with color, showing mosaic color-flow pattern with
high-velocity, low-impedance pulsatile flow, which is consistent with vascular
malformation rather than solid neoplasm.
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Fig. 8C —35-year-old man with renal arteriovenous malformation. Subsequent
gray-scale (B) and color Doppler (C) sonograms reveal anechoic
structures (arrows, B) in renal pelvis (excluding possibility
of solid mass), which fill with color, showing mosaic color-flow pattern with
high-velocity, low-impedance pulsatile flow, which is consistent with vascular
malformation rather than solid neoplasm.
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Subepithelial Renal Pelvic Hematoma
Renal hemorrhage can occur secondary to anticoagulant therapy or vasculitis
and may form hematomas either in the perirenal soft tissues or in the renal
pelvis. Subepithelial renal pelvic hematomas are also called Antopol-Goldman
lesions [20]. These are rare
lesions that usually present with hematuria and flank pain. To our knowledge,
only 28 cases have been described in the literature, of which only one was
managed conservatively. On CT, these hematomas appear as nonenhancing
heterogeneously dense or hyperdense masses in the renal pelvis that may cause
extrinsic luminal narrowing (Figs.
9A,
9B,
9C). They closely mimic renal
pelvic malignancy; the correct diagnosis is revealed in most cases only after
nephrectomy (Fig. 9D).
Awareness of and a high index of suspicion for an Antopol-Goldman lesion can
avoid an unnecessary nephrectomy, especially in patients with a nonenhancing
renal pelvic mass causing extrinsic compression on the collecting system who
have an underlying history of coagulopathy.
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Fig. 9D —35-year-old woman with subepithelial renal pelvic hematomas. Cut
section of surgically removed kidney shows multiple organizing hematomas
(arrow) and thromboemboli (arrowhead) in hilar adipose
tissue. Pathologic examination showed mass to be subepithelial renal pelvic
hematomas secondary to vasculitis.
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Extramedullary Hematopoiesis
Extramedullary hematopoiesis is a reactive process in response to the
failure of hematopoiesis in the bone marrow. It commonly occurs in the spleen,
liver, and lymph nodes; extramedullary hematopoiesis at other sites such as
the pleura, kidneys, gastrointestinal tract, breast, skin, brain, and adrenal
glands is uncommon. It commonly occurs in the presence of myelofibrosis with
myeloid metaplasia (most frequent), chronic myeloproliferative disorder,
polycythemia vera, and essential thrombocytosis. The presence of a renal mass
in association with any of these disorders should raise the possibility of an
extramedullary hematopoiesis.
Extramedullary hematopoiesis in the kidney occurs in three forms:
parenchymal, intrapelvic, and perirenal
[21]. A parenchymal type of
renal involvement appears as a diffuse enlargement of the kidney or as either
single or multiple small focal lesions. Pelvic involvement is either an
extension of parenchymal involvement or is isolated. In the perirenal type of
renal extramedullary hematopoiesis, a single hypoattenuating mass or multiple
nodules may be seen either around or completely encasing the kidneys
[22] (Figs.
10A,
10B and
10C). Biopsy confirmation is
usually required in extramedullary hematopoiesis
(Fig. 10D) to help to
differentiate it from lymphoma or urothelial tumors, which are often the first
diagnoses in such patients
[21]. But extramedullary
hematopoiesis should be considered high in the differential diagnosis when a
renal mass or masses are present in association with the previously mentioned
hematologic disorders.
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Fig. 10A —82-year-old woman with renal extramedullary hematopoiesis. Axial
(A) and coronal (B) unenhanced CT scans of right kidney show
multiple perirenal masses (arrowheads) with severe splenomegaly
(SP).
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Fig. 10B —82-year-old woman with renal extramedullary hematopoiesis. Axial
(A) and coronal (B) unenhanced CT scans of right kidney show
multiple perirenal masses (arrowheads) with severe splenomegaly
(SP).
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Fig. 10C —82-year-old woman with renal extramedullary hematopoiesis. Axial CT
scan of pelvis at bone window setting shows coarsening of bone matrix and
thinning of cortices, which are suggestive of extramedullary
hematopoiesis.
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Fig. 10D —82-year-old woman with renal extramedullary hematopoiesis.
Microscopy is characterized by presence of megakaryocytes (red arrow)
(confirmation by positive immunostaining for factor VIIIra) and granulocyte
precursors (blue arrow) (confirmation by positive Leder staining).
Presence of these blood cell precursors suggests hematopoietic process in
these masses. These microscopic features are confirmatory for extramedullary
hematopoiesis. (H and E, x40)
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Other entities that may present as renal pseudotumors but are not discussed
in this article include crossed fused renal ectopia, renal tuberculosis,
anticoagulant-induced subcapsular hemorrhage, and regenerating nodule after
reflux.
Conclusion
Many renal lesions may mimic renal cell carcinoma on radiologic imaging.
However, a high index of suspicion for renal pseudotumors as illustrated in
this article may help avoid unnecessary additional imaging and urologic
interventions.
References
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Abstract
Introduction
