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Anomalies of position

  1. Ectopic kidney—typically sited caudal to usual site. A pelvic
    kidney is due to failure of renal ascent. Blood supply is from the
    iliac artery or aorta. Most ectopic kidneys are asymptomatic,
    although pelvic kidneys are more susceptible to trauma, reflux,
    stone formation, PUJ obstruction and infection, and may
    complicate natural childbirth later in life. Rarely, a kidney may
    herniate through a Bochdalek hernia during its ascent, giving rise
    to an intrathoracic kidne


Anomalies of form

  1. Horseshoe kidney—two kidneys joined by parenchymal/fibrous
    isthmus, typically at the lower poles. Ascent is arrested by the
    inferior mesenteric artery. Most common fusion anomaly (1 in 400
    births). Both kidneys are malrotated with the renal pelves and
    ureters situated anteriorly and renal long axis medially oriented.
    Associated with many congenital syndromes (e.g. Turner) and an
    increased risk of malignancy (Wilms, TCC, RCC).
  2. Crossed renal ectopia—kidney is located on opposite side of
    midline from its ureteral orifice. Usually L→R. The lower kidney is
    usually ectopic. In 90% there is fusion of both kidneys (crossed
    fused ectopia).
  3. Pancake/discoid kidney—bilateral fused pelvic kidneys, usually
    near the aortic bifurcation.
  4. Renal hypoplasia—incomplete development results in a smaller
    kidney (<50% of normal size) with fewer calyces and papillae.
    Normal function


Anomalies of number

  1. Unilateral renal agenesis—1 in 1000 live births. Associated with
    chromosomal abnormalities, VACTERL anomalies, Müllerian duct
    anomalies (in women) and Zinner syndrome (in men: renal
    agenesis + ipsilateral seminal vesicle cyst + ejaculatory duct
    obstruction). Hyperplastic normal solitary kidney—up to twice the
    normal size.
  2. Bilateral renal agenesis—Potter syndrome. 1 in 10,000 live births.
    Invariably fatal in first few days of life due to pulmonary hypoplasia
    secondary to the associated oligohydramnios.
  3. Supernumerary kidney—very rare. Most commonly on left side
    caudal to normal kidney. May be partially fused with the normal
    kidney mimicking a duplex kidney, but the two components will
    have separate arterial and venous supply


  1. Cyst—well-defined nephrographic defect with a thin wall on the
    outer margin. Beak sign. Displacement and distortion of smooth-walled calyces without obliteration.
  2. Tumour—mostly RCC in adults and Wilms tumour in children.
  3. Fetal lobulation—the lobule directly overlies a normal calyx. Normal interpapillary line.
  4. Dromedary hump—on the midportion of the lateral border of the left kidney. Due to prolonged pressure by the spleen during fetal development. The arc of the interpapillary line parallels the renal contour.
  5. Splenic impression—on the left side only, producing an apparent bulge inferiorly.
  6. Enlarged septum of Bertin—overgrowth of the renal cortex from two adjacent renal lobules. Usually between upper and interpolar portion. Excretory urography shows a pseudomass with calyceal splaying and associated short calyx ± attempted duplication. DMSA accumulates normally or in excess. On US echogenicity is usually similar to the normal renal cortex but may be increased. CT and contrast-enhanced US, enhances similar to
    the cortex.
  7. Localized compensatory hypertrophy—e.g. adjacent to an area of pyelonephritic scarring.
  8. Acute focal nephritis (lobar nephronia)—usually an ill-defined hypoechoic mass on US, but may be hyperechoic. CT shows an ill-defined, low-attenuation, wedge-shaped mass with reduced contrast enhancement.
  9. Abscess—loss of renal outline and psoas margin on the control film. Scoliosis concave to the involved side. Initially there is no nephrographic defect, but following central necrosis there will be a central defect surrounded by a thick irregular wall. Adjacent calyces are displaced or effaced.
  10. Nonfunctioning moiety of a duplex—usually a hydronephrotic upper moiety. Delayed films may show contrast medium in the upper moiety calyces. Lower moiety calyces display the ‘drooping lily’ appearance



  1. Reflux nephropathy—focal cortical scar over a dilated calyx.
    Usually multifocal and may be bilateral. Scarring is most prominent
    at the upper and lower poles.
  2. Tuberculous autonephrectomy (putty kidney)—calcification
    differentiates it from the other members of this section.
  3. Lobar infarction—a broad contour depression over a normal
    calyx. Normal interpapillary line.
  4. Renal dysplasia—a forme fruste of multicystic kidney. Dilated
    calyces. Indistinguishable from chronic pyelonephritis.

Differential diagnosis
1. Persistent fetal lobulation—lobules overlie calyces with
interlobular septa between the calyces. Normal size kidney.




Prerenal = vascular
Usually with a small volume collecting system. This is a sign of
diminished urinary volume and, together with global cortical
thinning, delayed opacification of the calyces, increased density of
the opacified collecting system and delayed washout following
oral fluids or diuretics, indicates ischaemia.
1. Ischaemia due to renal artery stenosis—ureteric notching (due
to enlarged collateral vessels) differentiates this from the other
causes in this group. See Section 9.25.
2. Radiation nephritis—at least 23 Gy over 5 weeks. The collecting
system may be normal or small. Depending on the size of the
radiation field, both, one or just part of one kidney may be
3. End result of renal infarction—due to previous renal artery
occlusion or renal vein thrombosis. The collecting system does not
usually opacify during excretion urography.
Renal = parenchymal
1. Congenital hypoplasia—<6 calyces. The pelvicalyceal system is
otherwise normal.
2. Multicystic dysplastic kidney (adult).
3. Papillary necrosis—late sequela. See Section 9.23.
4. Postinflammatory—following acute diffuse nephritis especially in
5. Following partial nephrectomy.
Postrenal = collecting system
Usually with a dilated collecting system.
1. Postobstructive atrophy—± thinning of the renal cortex and if
there is impaired renal function this will be revealed by poor
contrast medium density in the collecting system.




Prerenal = vascular
1. Arterial hypotension—distinguished by the time relationship to
the contrast medium injection and its transient nature.
2. Generalized arteriosclerosis—normal calyces.
Renal = parenchymal
1. Chronic glomerulonephritis—normal calyces. Reduced
nephrogram density and poor calyceal opacification.
2. Hereditary nephropathies—e.g. Alport’s syndrome.
Postrenal = collecting system
1. Chronic papillary necrosis—with other signs of necrotic papillae




Prerenal = vascular
1. Acute renal vein thrombosis—enlarged kidney + surrounding
oedema + filling defect in the renal vein (best seen on CT). On US
the kidney may be hyper- or hypoechoic ± absent Doppler venous
flow ± visible thrombus. Echogenic streaks may be seen radiating
from the renal hilum (representing thrombosed veins). Most
common causes are nephrotic syndrome (in adults) and
dehydration/sepsis (in children). Many other causes including
intrinsic renal diseases (pyelonephritis, glomerulonephritis,
amyloid), hypercoagulable states (pregnancy, OCP, malignancy,
thrombophilia), extrinsic compression (by tumour, nodes or RPF),
vasculitis, sickle cell disease, trauma, transplant rejection. Beware
of tumour thrombus due to renal vein invasion from RCC—
this shows enhancement, whereas bland thrombus is
2. Acute arterial infarction—well-defined wedge-shaped areas of
reduced Doppler flow on US and reduced enhancement on CT.
Usually embolic, may be bilateral.Adrenals, urinary tract, testes and prostate 239
Renal = parenchymal
1. Duplex kidney—50% are bigger than the contralateral kidney;
40% are the same size; 10% are smaller.
2. Compensatory hypertrophy—for an atrophic/absent contralateral
3. Crossed fused ectopia—see Section 9.4.
4. Acute pyelonephritis—impaired excretion of contrast medium ±
dense nephrogram. Attenuated calyces but may have
nonobstructive pelvicalyceal or ureteric dilatation. Completely
reversible within a few weeks of clinical recovery.
5. Diffuse infiltrative tumour—e.g. lymphoma/leukaemia (usually
6. Malakoplakia—renal involvement may be diffuse causing enlargement.
Postrenal = collecting system
1. Obstructed kidney—dilated calyces and renal pelvis.
2. Xanthogranulomatous pyelonephritis—staghorn calculus is
typically present with dilated calyces and a contracted renal pelvis
(bear’s paw appearance) ± distortion of the renal outline and
perinephric stranding.
3. Pyonephrosis—obstructed kidney + echogenic pus in collecting
system + urothelial thickening




1. Bilateral duplex kidneys.
2. Autosomal recessive polycystic kidney disease—infantile form.
On US, smooth enlarged hyperechoic kidneys with numerous tiny
cysts and echobright foci.
1. Acute glomerulonephritis—many different causes including
Wegener’s granulomatosis, microscopic polyangiitis, Goodpasture’s
syndrome, SLE, HSP, infections, drugs. Renal cortex may be
diffusely hyperechoic on US.240 Aids to Radiological Differential Diagnosis
2. Acute tubular necrosis—usually due to hypoperfusion or toxins
(e.g. drugs, iodinated contrast, haemolysis, rhabdomyolysis).
Hyperechoic (or normal) renal cortex on US. Persistent
nephrogram on delayed postcontrast CT.
3. Acute cortical necrosis—>50% of cases are related to pregnancy
(placental abruption, infected abortion, preeclampsia). Other
causes include shock, sepsis, trauma, hyperacute transplant
rejection, HUS, sickle cell disease, NSAIDs. Enhancing medulla and
renal capsule with nonenhancing cortex on CT. Hypoechoic renal
cortex on US. Cortical calcification is a late finding.
4. Acute interstitial nephritis—most commonly an allergic drug
reaction. Other causes include autoimmune disease, acute
transplant rejection and various infections. Renal cortex may be
hyperechoic on US.
5. Polyarteritis nodosa—microaneurysms of renal artery branches +
small renal infarcts.
Deposition of abnormal proteins
1. Amyloid—secondary > primary amyloid. Kidneys may be enlarged
in acute disease ± focal mass lesions. Chronic deposition results in
small kidneys ± amorphous calcifications.
2. Multiple myeloma
—kidneys may be enlarged ± focal masses.
Usually in the setting of disseminated skeletal disease.
Neoplastic infiltration
Leukaemia and lymphoma—usually bilateral.
1. Bilateral hydronephrosis.
2. Acute renal papillary necrosis (see Section 9.23).
3. Acute uric acid nephropathy/tumour lysis syndrome—massive
tumour lysis following chemotherapy results in acute kidney injury
due to precipitation of uric acid and calcium phosphate crystals in
the renal tubules. Usually occurs in the setting of advanced
lymphoma or leukaemia. CT may show enlarged kidneys with
acute stone formation and/or milk of calcium in the collecting
systems ± obstruction.
4. Early diabetic nephropathy—renal echotexture is usually normal.
5. Sickle cell anaemia
—in early disease. The renal pyramids are
often echobright on US ± papillary necrosis. The kidneys atrophy
in chronic disease.
6. HIV-associated nephropathy—bilateral enlarged hyperechoic
kidneys + urothelial thickening ± effacement of renal sinus fat.
7. Acromegaly* and gigantism—as part of the generalized
visceromegaly. Tall stature, obesity and steroid use can also result
in large kidneys with normal echotexture



Dystrophic calcification due to localized disease

  1. Infections
    (a) Chronic pyelonephritis—focal unilateral/asymmetrical cortical
    calcification with associated parenchymal scarring. Pyogenic
    abscesses can rarely calcify.
    (b) Tuberculosis*—variable appearance of nodular, curvilinear or
    amorphous calcification, usually within dilated calyces or
    tuberculous abscess → end-stage putty kidney. Typically
    multifocal with calcification elsewhere in the urinary tract. In
    the early stage there may be triangular ring-like medullary
    calcification due to papillary necrosis. The urogenital tract is
    the second commonest site of involvement after the lungs.
    (c) Xanthogranulomatous pyelonephritis—large obstructive
    calculus in 80% of cases.
    (d) Hydatid—the cyst is usually polar and calcification is curvilinear
    or heterogeneous. 50% of echinococcal cysts calcify.
  2. Tumours—e.g. RCC, Wilms tumour, TCC, metastasis.
  3. Cysts—rim/septal calcification, usually related to previous infection
    or haemorrhage. Common in ADPKD.
  4. Vascular—e.g. in a chronic perinephric haematoma, or curvilinear
    calcification in atherosclerotic/aneurysmal renal arteries.
Calcium oxalapte/phosphate 75%
Pure ca oxalate
Struvite 15%
Uric acid
Xanthine -RL

75% are calcium oxalate/phosphate. Usually very dense (up to
1700 HU on CT). Causes include:
1. With normocalcaemia—obstruction, UTI, prolonged bed rest,
dehydration, congenital renal anomalies (e.g. horseshoe kidney),
calyceal/bladder diverticula, Cushing’s syndrome, type 1 renal
tubular acidosis, medullary sponge kidney, idiopathic
2. With hypercalcaemia—hyperparathyroidism, milk-alkali syndrome,
excess vitamin D, sarcoidosis, idiopathic infantile hypercalcaemia.

Pure calcium oxalate
Due to hyperoxaluria. Can lead to oxalosis (deposition of oxalate
in extrarenal organs) if untreated.
1. Secondary hyperoxaluria—mainly in patients with Crohn’s
disease, small bowel resection, high vitamin C intake or chronic
renal failure/dialysis.
2. Primary hyperoxaluria—rare, autosomal recessive, typically
presents in childhood. Radiologically: cortical and medullary
nephrocalcinosis (generally diffuse and homogeneous), recurrent
renal stones, dense vascular calcification, osteopenia or renal
osteodystrophy and abnormal metaphyses (dense/lucent bands).

Account for 15% of calculi overall, and 70% of staghorn calculi.
Caused by urease-producing bacterial UTI (e.g. Proteus, Klebsiella,
Pseudomonas, Enterobacter—not E. coli); more common in women.

Due to inherited cystinuria, presents in younger patients. Stones
are usually <550 HU on CT, often large in size (may be staghorn)
and homogeneous in density.

Uric acid
Usually <500 HU on CT, typically form in acidic urine. Causes
1. With hyperuricaemia—gout, myeloproliferative disorders and
tumour lysis syndrome.
2. With normouricaemia—idiopathic or associated with acidic,
concentrated urine, e.g. in hot climates and in chronic diarrhoea
(including ileostomy patients).

Rare, due to xanthinuria, which may be primary (hereditary
xanthinuria) or secondary (due to allopurinol). Stones are
radiolucent on plain film but radiopaque on CT


Stones radiolucent on CT (soft-tissue attenuation)

Rare. Suspect in patients with ureteric obstruction without a
visible cause on unenhanced CT. CT urography will show the
stone as a filling defect

  1. Protease inhibitors, e.g. Indinavir—used in HIV treatment. Most
    common medication-induced calculus—other causes include
    sulphonamides, ciprofloxacin, ephedrine, guaifenesin.
  2. Matrix—mainly composed of mucoproteins. Tend to occur in
    patients with a history of UTIs, renal stones or proteinuria on




Nonstone genitourinary
1. Pyelonephritis—asymmetric perinephric stranding or mild renal
enlargement. Mild disease may have no signs on unenhanced CT.
Post IV contrast, pyelonephritis may be seen as a focal region of
low attenuation or a more widespread striated enhancement of the
kidney. Renal or perinephric abscesses are rare sequelae.
2. Congenital PUJ obstruction—hydronephrosis with a sudden
transition to normal at the PUJ without a visible cause on CT.
3. Ureteric obstruction by any other cause.
4. Cystitis.
5. Renal neoplasm—e.g. RCC, TCC.
6. Perinephric/subcapsular haemorrhage—if no history of trauma
or coagulopathy, consider the possibility of an underlying tumour.
7. Renal infarction or renal vein thrombosis—difficult to appreciate
on unenhanced CT. Perinephric stranding may be the only visible
sign. Acute thrombus within the renal vein may appear
hyperattenuating compared to flowing blood in the IVC.
1. Adnexal masses—most commonly ovarian cysts (usually
haemorrhagic), tuboovarian abscesses, dermoid cysts,
endometriomas and ovarian neoplasms.
2. Cervical cancer—which may involve the distal ureters.
3. Degenerating or torted fibroids.
4. Ectopic pregnancy.
1. Appendicitis—if pain is right-sided.
2. Diverticulitis—usually left-sided. Meckel’s diverticulitis may occur
on either side.
3. Abdominal hernias—particularly inguinal.
4. Fat necrosis—e.g. epiploic appendagitis (usually left-sided) or
omental infarction (usually right-sided).
5. Other bowel pathology—e.g. obstruction, intussusception,
ischaemia, IBD or tumour.Adrenals, urinary tract, testes and prostate 245
Pancreatic and hepatobiliary disorders
1. Gallstones.
2. Pancreatitis and pancreatic tumours.
1. Renal artery aneurysm.
2. Ruptured abdominal aortic aneurysm—a crescent-shaped area of
high attenuation (> intraluminal blood) in the wall of an AAA on
unenhanced CT is a sign of impending rupture. Periaortic
stranding or haemorrhage (>60 HU) indicates active bleeding.
3. Aortic dissection—high attenuation in the aortic wall on
unenhanced CT indicates intramural haematoma. Displacement of
intimal calcification into the aortic lumen and/or renal infarction
may be seen.
4. SMA thrombosis, embolism or dissection—pain may radiate to
one side. Difficult to appreciate on unenhanced CT, may see vessel
enlargement, perivascular stranding, high-attenuation blood clot
within the vessel or displacement of intimal calcification (in the
case of dissection) + signs of bowel ischaemia.
5. Intraperitoneal and retroperitoneal haemorrhage—e.g. due to
trauma, anticoagulants, coagulopathy, vasculitis (PAN), splenic
rupture and certain neoplasms.
6. Rectus sheath haematoma—hyperattenuating compared with
normal muscle on unenhanced CT. Usually due to anticoagulants/
1. Mechanical low back pain.
2. Osteoporotic fracture—usually in the elderly.
3. Bone metastases and myeloma.
4. Psoas haematoma.
5. Discitis—difficult to appreciate on unenhanced CT. May see
endplate irregularity and fat stranding adjacent to a disc



Medullary (pyramidal)

  1. Medullary sponge kidney—developmental anomaly causing cystic
    dilatation of the small collecting ducts in the medullary pyramids;
    may involve a variable portion of one or both kidneys. The dilated
    tubules fill with contrast during an IVU, giving a characteristic
    ‘paintbrush’ appearance to the pyramids. The tubules may contain
    small calculi, giving rise to medullary nephrocalcinosis—this usually
    manifests as focal or asymmetrical clusters of punctate calcification.
    Kidneys may be enlarged or normal in size. Echobright medullary
    pyramids on US (even without calcification). MRI may show cystic
    nature of pyramids on T2 sequences. Associated with Caroli disease
    of the liver.
  2. Hyperparathyroidism*—usually bilateral and symmetrical, diffuse
    rather than punctate.
  3. Renal tubular acidosis (type 1)—most common cause in children,
    may be associated with osteomalacia or rickets. Calcification tends
    to be more severe and confluent than in other causes; typically
    bilateral and symmetrical. Kidneys are usually of normal size.
  4. Renal papillary necrosis—calcification of necrotic papillae. Usually
    asymmetrical. See Section 9.23.
  5. Causes of hypercalcaemia or hypercalciuria—e.g. malignancy
    (bone metastases, myeloma, paraneoplastic syndromes),
    sarcoidosis, hypervitaminosis D, milk-alkali syndrome and
    idiopathic hypercalciuria.
  6. Preterm neonates—in up to two-thirds. Risk factors include
    extreme prematurity, severe respiratory disease, gentamicin use,
    and high urinary oxalate and urate excretion. Echobright
    medullary pyramids on US, typically bilateral and symmetrical. The
    majority resolve spontaneously by midchildhood. Main differential
    in this patient group is papillary necrosis, which also produces
    echobright medullary pyramids but is usually asymmetrical and
    results in sloughing of papillae within weeks.
  7. Hyperoxaluria—typically causes diffuse cortical and medullary
    nephrocalcinosis as well as nephrolithiasis. Primary form presents in
  1. Acute cortical necrosis—classically ‘tramline’ calcification, occurs
    in the chronic phase.
  2. Chronic glomerulonephritis—bilateral curvilinear or punctate
    cortical calcification.
  3. Chronic infection—multifocal nodular cortical calcification can
    occur with HIV-related renal infections, e.g. Pneumocystis jirovecii,
    Mycobacterium avium complex (MAC) and CMV.
  4. Chronic renal transplant rejection—due to cortical necrosis.
  5. Hyperoxaluria—typically causes diffuse cortical and medullary
  6. Alport syndrome—rare inherited disorder (most commonly
    X-linked), presents in adolescence or early adulthood with
    progressive renal failure and deafness. Renal calcification can look
    identical to hyperoxaluria


Renal dysplasia

  1. Multicystic dysplastic kidney—due to ureteric atresia during early
    fetal life; usually diagnosed antenatally. Multiple cysts replace the
    kidney with intervening echobright dysplastic tissue (no
    functioning renal tissue). Typically involutes over time. Associated
    with contralateral PUJ obstruction (PUJO) and reflux. Typically
    involves the whole kidney but can rarely be segmental (in the case
    of a duplex kidney with antenatal atresia of only one ureter),
    thereby mimicking a multiloculated cystic mass.
  2. Localized cystic renal disease—a nonencapsulated cluster of
    variable-sized cysts replacing part of one kidney. May occasionally
    involve the entire kidney but is always unilateral.


Polycystic kidney disease*

  1. Autosomal recessive polycystic kidney disease*—presents
    antenatally or in infancy/childhood. Bilateral enlarged echogenic
    kidneys with multiple microcysts, most of which are too small to
    resolve individually (often seen as tiny echobright foci). See Part 2
    for other features and associations.
  2. Autosomal dominant polycystic kidney disease*—usually
    presents in adulthood (or earlier if undergoing screening). Enlarged
    kidneys with numerous cysts of varying sizes. See Part 2 for other
    features and associations

Cystic tumours

  1. Multilocular cystic nephroma—nonhereditary, benign. Usually
    presents in young children (not neonates) or middle-aged women.
    Multilocular cystic mass with a fibrous capsule. Linear septal and
    capsular enhancement is often seen on CT/MRI, but nodular
    enhancement should not be present. Cannot be reliably
    differentiated from cystic RCC.
  2. Multilocular cystic RCC—5% of RCCs are cystic (variant of clear
    cell RCC). Nodular components on imaging suggest RCC.
  3. Mixed epithelial and stromal tumour—rare, typically seen in
    perimenopausal women particularly those taking OCP/hormone
    replacement therapy. Complex multiloculated cystic mass on
    imaging, often with enhancing nodular components ± calcification.
    Indistinguishable from cystic RCC on imaging.
  4. Angiomyolipoma with epithelial cysts—rare cystic variant of
    AML. Indistinguishable from cystic RCC on imaging.
  5. Primary renal sarcoma—e.g. leiomyosarcoma, angiosarcoma. Rare
    and aggressive, usually solid but can occasionally be predominantly
    cystic with enhancing nodular components.
  6. Cystic Wilms tumour—extremely rare in adults

Cortical cysts

  1. Simple cyst—unilocular, thin-walled, no enhancement. Increase in size and number with age. May become haemorrhagic (>20 HU on unenhanced CT) or infected (thickened enhancing wall ±septations).
  2. Syndromes associated with cysts
    (a) von Hippel-Lindau disease—most patients will have renal cysts. There is also a high risk of RCC, many of which arise from preexisting cysts. Even simple-looking cysts on imaging often contain foci of RCC on histology. Fortunately, RCCs in vHL are slow growing and typically do not metastasize until they are >3 cm, therefore cysts can be followed up to look for
    malignant transformation.
    (b) Tuberous sclerosis
    —cysts are the second most common renal manifestation after angiomyolipomas.
  3. End-stage renal disease and haemodialysis—causes interstitial
    fibrosis and hyperplasia of tubular epithelium leading to cyst
    formation. On imaging: atrophic kidneys containing multiple cysts
    (>2 on each side) of varying size ± internal haemorrhage ± rupture.
    Incidence increases with time on dialysis, but cysts usually involute
    after a successful renal transplant. Also increased risk of RCC (7%,
    usually papillary type), increasing with time on dialysis.
  4. Lithium-induced nephrotoxicity—causes chronic focal interstitial nephritis. Numerous 1–2 mm cortical and medullary cysts in normal-sized kidneys. On US these are often seen as multiple tiny echobright foci (rather than anechoic cysts) due to their small size, and may be mistaken for calcification.
  5. Glomerulocystic kidney disease—rare, usually presents in
    children. Multiple bilateral small cysts in a characteristic subcapsular cortical distribution, due to cystic dilatation of Bowman’s capsule. The cysts may be difficult to visualize on US due to their small size and are best seen on T2-weighted MRI


Medullary cysts

  1. Calyceal diverticulum—solitary unilocular cystic space
    communicating via an isthmus with the fornix of a calyx. Fills with
    contrast during excretion urography. May contain milk of calcium
    or dependent calculi—highly suggestive of a diverticulum. Risk of
    infection, bleeding and rupture.
  2. Medullary sponge kidney—bilateral in 60%–80%. Multiple tiny
    cysts in the medullary pyramids that opacify during excretion
    urography (‘paintbrush’ appearance) and often contain tiny calculi.
    The cysts themselves are usually too small to see on US, and cause
    a generalized increase in medullary echogenicity.
  3. Papillary necrosis—clubbed calyces may mimic cysts on US.
  4. Medullary cystic disease complex—refers to two clinically similar
    inherited disorders presenting with polyuria and polydipsia (due to
    salt-wasting) and progressive renal failure. Adult form (medullary
    cystic kidney disease) presents at 20–40 years. Juvenile form
    (juvenile nephronophthisis) presents in children. US shows normal/
    small echobright kidneys with multiple small cysts in the medulla
    and corticomedullary junction.



  1. Infective
    (a) Pyogenic abscess—complex cystic lesion with internal echoes
    on US and a thick irregular wall on CT ± internal gas. May be
    within the kidney or perinephric. Renal aspergillosis and
    actinomycosis can have identical appearances but occur in
    immunocompromised patients (including diabetics and those
    on steroid therapy).
    (b) Xanthogranulomatous pyelonephritis—gross cystic dilatation
    of multiple calyces may mimic a complex cystic mass but the
    presence of a large renal pelvic calculus aids diagnosis.
    (c) Tuberculosis*—causes papillary necrosis and infundibular
    stenosis resulting in dilated moth-eaten or clubbed calyces +
    calcification (late stage). These can be large and mimic a cyst.
    Tuberculous abscesses can also form if the caseating papillary
    necrosis does not rupture into the collecting system.
    (d) Hydatid cyst—rare. Initially unilocular, later becoming
    multilocular and thick-walled due to the formation of daughter
    cysts. The lesion becomes semisolid and calcified after death
    of the parasite.
    (e) Candidiasis—rare, seen in immunocompromised patients.
    Typically causes multiple microabscesses, also involves the liver
    and spleen.250 Aids to Radiological Differential Diagnosis
  2. Traumatic—intrarenal haematoma or urinoma.
  3. Endometriosis*—renal involvement is rare, usually presents with a
    complex haemorrhagic cystic lesion.


Extraparenchymal renal cysts

  1. Parapelvic cyst—essentially just a cortical cyst that extends into
    the renal sinus fat. Usually single and unilateral but may be
    multiple. Large cysts may cause haematuria, hypertension or
    hydronephrosis via local compression.
  2. Peripelvic cyst— also known as renal sinus cyst or lymphangioma.
    Arises from dilated lymphatics in the renal sinus, thus does not
    involve the renal parenchyma. Usually multiple, small and bilateral;
    elongated simple cysts that do not communicate with the
    collecting system. Mimics hydronephrosis but can be differentiated
    on excretory phase CT. Lymphangiomatosis may also present with
    bilateral perinephric cystic lesions


  1. Angiomyolipoma—the vast majority of renal lesions containing
    macroscopic fat (4 cm or with intralesional aneurysms >5 mm. May rarely extend
    into the renal vein ± IVC. AMLs are seen in up to 80% of patients
    with tuberous sclerosis; usually multiple, bilateral, large and often
    fat-poor. Can also be seen in LAM, NF1 and vHL.
  2. Renal cell carcinoma—microscopic fat is very common (in up to
    60%), seen as signal dropout on out-of-phase MRI sequences.
    Macroscopic fat (i.e. visible on CT) is rare, but the presence of
    both macroscopic fat and calcification within a renal mass suggests
    RCC since calcification is very rare in AML.
  3. Liposarcoma—arises from perinephric/retroperitoneal fat. Usually
    large, displaces and compresses the adjacent kidney. Can mimic an
    exophytic AML, but helpful features favouring AML include a renal
    cortical defect (representing the site of origin of the AML) and
    prominent intratumoural vessels extending into the renal cortex.
  4. Lipoma—rare. Composed entirely of fat, no soft-tissue component.
    Similar on CT to a fat-rich AML.
  5. Oncocytoma—can rarely contain a small focus of macroscopic fat.
  6. Xanthogranulomatous pyelonephritis—xanthomatous material
    within dilated calyces can be of low attenuation on CT similar to
    fat density.
  7. Wilms tumour—very rare in adults.
  8. Teratoma—very rare, usually found in children or adolescents.
    Contains varying amounts of soft tissue, fat and calcification. A
    fat–fluid level is characteristic.
  9. Renal sinus lipomatosis—expansion of the renal sinus fat without
    a soft-tissue component, secondary to chronic inflammation


Well-defined mass

  1. Renal cell carcinoma—90% of malignant renal tumours in
    adults. Multiple or bilateral in 3%–5% (common in polycystic
    kidneys and vHL). Typically well-defined, may contain 254 Aids to Radiological Differential Diagnosis
    calcification. May be hyperechoic on US, mimicking AML (a
    hypoechoic rim and heterogeneous echotexture favour RCC, but
    there is significant overlap). In practice all solid well-defined renal
    masses are presumed to be RCC due to its frequency and varied
    appearance. Invades renal vein/IVC in advanced stage.
    Appearance depends on subtype:
    (a) Clear cell—most common (80%). Avid heterogeneous
    arterial enhancement ± washout in the nephrographic phase.
    Frequently contains cystic, haemorrhagic or necrotic
    components. Up to 60% contain microscopic fat on in/out
    of phase MRI, but macroscopic fat (on CT) is rare. Typically
    T2 hyperintense.
    (b) Papillary—10%–15% of RCCs, most common form in
    dialysis patients. Often multiple and bilateral in hereditary
    papillary RCC syndrome. Typically homogeneous, T2
    hypointense and hypovascular with only mild enhancement
    on CT/MR. Can mimic hyperdense cyst on CT (enhancement
    in papillary RCC may be very subtle; precontrast T1
    hyperintensity on MRI can help confirm haemorrhagic cyst)
    and fat-poor AML (but microscopic fat on MRI is rare in
    papillary RCC and common in fat-poor AMLs).
    (c) Chromophobe—5% of RCCs, best prognosis. Often multiple
    in Birt-Hogg-Dubé syndrome. Shows moderate enhancement
    on CT/MR, which may be homogeneous or heterogeneous.
    Variable T2 signal, may have a T2 hyperintense central
    fibrous scar which shows delayed enhancement, mimicking
    oncocytoma—DWI may be helpful (chromophobe RCCs tend
    to restrict diffusion more than oncocytomas) but not enough
    to accurately differentiate the two.
  2. Oncocytoma—most common benign solid nonfatty renal mass,
    usually solitary and unilateral except in Birt-Hogg-Dubé
    syndrome, hereditary oncocytosis and some cases of tuberous
    sclerosis. Typically shows homogeneous early enhancement
    followed by washout. May have a hypovascular T2 hyperintense
    central fibrous scar which shows delayed enhancement. Cannot
    be reliably differentiated from RCC (particularly chromophobe
    type) therefore is often resected.
  3. Fat-poor angiomyolipoma—5% of AMLs do not contain
    macroscopic fat visible on CT (particularly in tuberous sclerosis),
    although many of these will have microscopic fat on in/out of
    phase MRI. Usually hyperattenuating on unenhanced CT (>45
    HU) with homogeneous enhancement. Typically T2 hypointense
    on MRI + restricted diffusion. Hard to differentiate from papillary
    RCC, although the presence of microscopic fat suggests AML
    (rare in papillary RCC). Epithelioid AML is an aggressive variant
    that is fat-poor, often bleeds, has malignant potential
    and is frequently associated with tuberous sclerosis.Adrenals, urinary tract, testes and prostate 255
  4. Haemangioma—rare, small, nearly always arises from the renal
    papillae or pelvis. More common in young adults, including
    those with Klippel-Trénaunay and Sturge-Weber syndromes.
    Usually shows avid peripheral enhancement persisting on later
    phases (no washout). Homogeneously T2 hyperintense on MRI.
    May contain phleboliths.
  5. Leiomyoma—rare, usually small and solitary. Most commonly
    arise from the renal capsule but can arise from the renal pelvis.
    Typically well-defined, homogeneously hyperattenuating on
    unenhanced CT with uniform enhancement, but may be
    heterogeneous if large. T1/T2 hypointense on MRI.
  6. Juxtaglomerular cell tumour—rare, benign, typically seen in
    young adults presenting with uncontrolled hypertension, polyuria
    and polydipsia due to renin secretion. Solitary well-defined
    hypovascular mass with heterogeneous delayed enhancement.
  7. Metanephric adenoma—rare benign tumour usually found in
    middle-aged patients. Polycythaemia is characteristic, but only
    found in 10% of patients. Well-defined hypovascular mass with
    heterogeneous enhancement ± haemorrhage, necrosis or
  8. Medullary fibroma—benign lesion found in the renal pyramid.
    Typically <5 mm and hypovascular, thus hard to see on imaging.
    Can rarely be large, presenting as a heterogeneous mass with
    low T1 and T2 signal protruding into the renal pelvis.
  9. Papillary adenoma—common premalignant lesion, particularly
    in dialysis patients. Typically subcapsular in location, hypovascular
    and <5 mm by definition, thus hard to see on imaging (usually
    found incidentally on histology).
  10. Sarcomas—rare and aggressive, most present as a large
    well-defined heterogeneous mass ± necrosis, haemorrhage or
    cystic change. Leiomyosarcoma is most common; other types
    include osteosarcoma (typically calcified), Ewing sarcoma (usually
    in children or adolescents), synovial sarcoma, fibrosarcoma, clear
    cell sarcoma. Note that large RCCs can undergo sarcomatoid
    transformation—this is more common than primary renal
  11. Other rare lesions not specific to the kidney—e.g. solitary
    fibrous tumour (relatively homogeneous enhancement, often has
    radial bands of low T2 signal on MRI), sarcoidosis (typically
    multifocal, T2 hypointense on MRI), inflammatory pseudotumour,
    plasmacytoma, glomus tumour, myopericytoma, schwannoma,
    paraganglioma, carcinoid. Most of these usually present as
    nonspecific well-defined heterogeneously enhancing masses
    indistinguishable from RCC.
  12. Pseudotumours—e.g. prominent column of Bertin, persistent
    fetal lobulation, dromedary hump, aneurysms and AVMs.
    Splenosis on the surface of the left kidney may also mimic a renal 256 Aids to Radiological Differential Diagnosis
    lesion, but the history of splenic trauma/resection and the
    enhancement pattern is usually diagnostic. Congenital
    splenorenal fusion (of heterotopic splenic tissue) can have a
    similar appearance but is very rare. Large adrenal masses
    inseparable from the kidney may also mimic a renal mass

Infiltrative lesions
ill-defined, hypovascular and do not usually distort the
renal contour

  1. Urothelial carcinoma (aka TCC)—typically ill-defined and
    hypovascular, arises from the pelvicalyceal system and may
    obstruct or obliterate other calyces. May seed further down the
    urinary tract. Early tumours are seen as a mildly enhancing
    polypoid or sessile filling defect in the pyelographic phase on
    IVU, CT or MR.
  2. Squamous cell carcinoma—usually associated with calculi or
    chronic UTI, can also occur in XGP. Starts as a plaque or stricture
    in the pelvicalyceal system but infiltrates the renal parenchyma
    early on, so there is usually a large parenchymal mass before any
    sizeable intrapelvic mass. May be very difficult to identify in
    chronically infected and distorted kidneys, e.g. in XGP.
  3. Infiltrative subtypes of RCC—medullary carcinoma (nearly
    always in young patients with sickle cell trait) and collecting duct
    carcinoma both typically have infiltrative growth patterns and are
    aggressive, often metastatic at presentation.
  4. Lymphoma*—usually secondary involvement in advanced NHL
    (primary lymphoma is very rare as there is no renal lymphoid
    tissue). Usually there are multifocal bilateral infiltrative
    hypovascular lesions on CT/MR, which are T2 hypointense, but
    can present as a single ill-defined mass, diffuse renal
    enlargement, perinephric soft-tissue thickening or direct
    extension from retroperitoneal lymphadenopathy. Can affect the
    renal sinus and mimic TCC.
  5. Metastases—not uncommon, usually in the presence of
    metastatic disease elsewhere. Ill-defined hypovascular mass or
    masses. Lung, breast, GI tract, melanoma and the contralateral
    kidney are the most common sources.
  6. Leukaemia—typically causes bilateral diffuse renal enlargement
    but can rarely present with single or multiple masses (chloroma
    in acute myeloid leukaemia).
  7. Malakoplakia—uncommon inflammatory condition usually
    involving the urinary tract, related to recurrent E. coli infection.
    Most commonly involves the urothelium (causing nodules or
    plaques), but can also involve the renal parenchyma causing
    focal, multifocal or diffuse infiltrative lesions. May extend into the
    perinephric fat.Adrenals, urinary tract, testes and prostate 257
  8. Sarcomas—rare. Angiosarcoma and rhabdomyosarcoma often
    have an infiltrative growth pattern.
  9. Other rare lesions—e.g. plasmacytoma, extramedullary
    haematopoiesis, inflammatory pseudotumour, Wegener’s
    granulomatosis, Rosai-Dorfman disease, amyloidosis.
  10. Mimics—focal pyelonephritis often presents as an ill-defined area
    of hypovascularity or striated enhancement, but the clinical
    features of sepsis are usually indicative. This is usually T2
    hyperintense on MRI and may be hypo- or hyperechoic on US.
    A renal infarct presents as a peripheral wedge-shaped
    hypovascular area (± renal capsule enhancement) and may be
    multifocal. Predisposing factors are usually present. Radiation
    nephritis (due to spinal or retroperitoneal radiotherapy) presents
    as a well-defined wedge of hypoenhancement in the medial
    aspect of one or both kidneys.


  1. Urothelial carcinoma—intraluminal filling defect on excretory
    urography, centred in the renal pelvis which secondarily invades
    the renal sinus and renal parenchyma. Commonly causes calyceal
  2. Squamous cell carcinoma—strongly associated with renal calculi
    and chronic UTI.
  3. Metastasis to sinus lymph nodes.
  4. Lymphoma*—may be limited to the renal sinus, particularly in
    PTLD. Ill-defined hypovascular mass which characteristically does
    not cause obstruction.
  5. Mesenchymal tumour—e.g. lipoma, medullary fibroma,
    haemangioma, leiomyoma.
  6. Retroperitoneal tumours extending into the renal sinus—any
    retroperitoneal tumour but lymphoma most commonly.
  7. Renal parenchymal tumours projecting into the renal


Nonneoplastic lesions

  1. Peripelvic cyst—typically multiple and bilateral, arise from
    lymphatics within sinus fat. See Section 9.15.
  2. Parapelvic cyst—single, larger cyst protruding into the sinus,
    originating from the adjacent parenchyma. See Section 9.15.
  3. Sinus lipomatosis—echogenic central sinus complex on US. CT
    and MRI directly reveal fatty nature.
  4. Vascular—renal artery aneurysm, AVM or renal vein varix can
    manifest as peripelvic lesions. Colour Doppler or contrast-enhanced
    CT are diagnostic.
  5. Inflammatory—soft-tissue thickening in the sinus due to chronic/
    severe pyelonephritis, XGP or malakoplakia.
  6. Haematoma—due to anticoagulants or less commonly trauma.
  7. Urinoma—due to pelvicalyceal rupture, usually associated with
    ureteral obstruction (e.g. stones), PUJ obstruction or trauma
    (including surgery).
  8. Rare infiltrative disorders—any of the following can cause
    bilateral infiltrative masses in the renal sinus ± hydronephrosis.
    (a) Rosai-Dorfman disease—renal involvement is rare but the
    most common manifestation is bilateral infiltrative renal hilar
    (b) Retroperitoneal fibrosis—periaortic soft tissue may extend
    into the renal sinus.
    (c) Erdheim-Chester disease
    —perinephric soft tissue may
    extend into the renal sinus.Adrenals, urinary tract, testes and prostate 259
    (d) Amyloidosis*—can rarely involve the renal sinuses, causing
    infiltrative soft-tissue masses which may calcify (highly
    (e) Extramedullary haematopoiesis—look for signs of bone
    marrow failure, e.g. bone sclerosis, splenomegaly. Uptake on
    sulphur colloid scintigraphy is diagnostic.

Soft-tissue rind

  1. Lymphoma*—usually due to extension of renal/retroperitoneal
    lymphoma into perinephric space, but can present as isolated
    perinephric soft-tissue thickening.
  2. Erdheim-Chester disease*—retroperitoneal involvement is
    common and produces a characteristic rind of soft tissue around
    the kidneys and aorta.
  3. Amyloidosis*—may diffusely infiltrate the perinephric and
    retroperitoneal fat ± foci of calcification (highly suggestive).
  4. Retroperitoneal fibrosis—periaortic soft tissue may extend into
    the perinephric space.
  5. Metastases—most present as focal masses but breast cancer can
    present as infiltrative retroperitoneal soft tissue, which can involve
    the perinephric space.
  6. Extramedullary haematopoiesis—can rarely infiltrate the
    perinephric fat.
  7. Rosai-Dorfman disease*—can rarely cause subcapsular renal
  8. Nephroblastomatosis—only occurs in infants and children, due to
    persistent nephrogenic rests. Presents as bilateral confluent
    subcapsular soft-tissue nodules, which are homogeneous and
    hypovascular. Risk of malignant transformation to Wilms tumour

Focal solid lesion

  1. Renal lesions extending into the perinephric space—e.g.
    tumours (RCC, TCC), inflammatory lesions (malakoplakia, XGP).
  2. Metastases—common sources include lung and melanoma. Usually in the presence of metastatic disease elsewhere. Lymphoma, leukaemia and myeloma may also rarely present as a focal perinephric mass.
  3. Perinephric haematoma—may be spontaneous (due to vasculitis,
    anticoagulation or coagulopathy) or due to an underlying aneurysm or mass lesion, e.g. AML or RCC. Hyperattenuating subcapsular mass that does not enhance post contrast.
  4. Nodular fat necrosis due to severe pancreatitis—usually presents with numerous small soft-tissue nodules (± central fat) throughout the intraabdominal fat.
  5. Primary sarcoma—some liposarcomas may present as a solid mass. Other sarcomas can also arise from the perinephric space.
  6. Other rare lesions not specific to the perinephric space—e.g.
    haemangioma, solitary fibrous tumour, Castleman disease, desmoid tumour, inflammatory pseudotumour, plasmacytoma.

Fatty lesions

  1. Exophytic angiomyolipoma—often large, mimics perinephric
    liposarcoma. Features favouring AML include a focal renal cortical
    defect (representing the site of origin) and prominent
    intratumoural vessels extending into the renal parenchyma.
  2. Liposarcoma—most common primary retroperitoneal malignancy,
    often arises from perinephric fat. Usually large and unencapsulated,
    displaces the adjacent kidney. See Section 4.4 for subtypes.
  3. Perinephric lipomatosis—associated with renal stones and chronic
    renal infection (including XGP and TB). Expansion of the
    perinephric and renal sinus fat ± stranding.
  4. Extraadrenal myelolipoma—can rarely arise from the perinephric
    space. Mimics liposarcoma due to mix of fatty and soft-tissue
    components, but typically appears encapsulated. Uptake on
    sulphur colloid scintigraphy suggests myelolipoma but is also seen
    in extramedullary haematopoiesis.
  5. Extramedullary haematopoiesis—may contain foci of
    macroscopic fat.

Cystic lesions

  1. Exophytic renal cyst or cystic lesions—including cystic neoplasms
    and abscesses.
  2. Urinoma—due to pelvicalyceal rupture, usually associated with
    ureteral obstruction (e.g. stones), PUJO or trauma/surgery.
  3. Lymphangiomatosis—rare benign lymphatic malformation
    resulting in bilateral multiloculated perinephric cysts and usually
    multiple bilateral peripelvic cysts


Absent nephrogram

  1. Global—nearly always due to main renal artery occlusion, either
    due to thrombosis, dissection or traumatic avulsion. Renal vein
    thrombosis can also give this appearance. A rim of capsular
    enhancement (‘rim nephrogram’) may be seen due to patent
    capsular vessels, usually developing several days after the initial
    vascular insult.
  2. Segmental—due to focal renal infarction (usually embolic
    or vasculitic), focal pyelonephritis or an infiltrative lesion.
    A rim of capsular enhancement, if present, indicates


Unilateral delayed nephrogram

  1. Obstructive uropathy—e.g. ureteric stone/tumour.
  2. Reduced arterial inflow—e.g. renal artery stenosis, Page kidney
    (reduced perfusion due to extrinsic compression by a subcapsular
    haematoma or collection).
  3. Reduced venous outflow—e.g. renal vein thrombosis or
  4. Pyelonephritis—although a striated nephrogram is more
    common. As opposed to the other differentials, pyelonephritis
    does not result in a progressively hyperdense nephrogram.

Bilateral persistent nephrogram
Both kidneys are still in the corticomedullary phase >90 seconds
or nephrographic phase >3 minutes after contrast injection.

  1. Reduced arterial inflow—e.g. systemic hypotension/shock, and
    rarely bilateral renal artery stenosis.
  2. Abnormal renal tubules—e.g. acute tubular necrosis (including
    iodinated contrast nephropathy), acute glomerulonephritis, acute
    papillary necrosis, tumour lysis syndrome or tubular protein
    deposition (myeloma, rhabdomyolysis, amyloidosis). In acute
    tubular necrosis the nephrograms may persist for days.
  3. Bilateral obstructive uropathy—rare.
  4. Reduced venous outflow—e.g. bilateral renal vein thrombosis.

Unilateral striated nephrogram
Streaky radial bands of alternating hyper and hypoattenuation,
best seen in the excretory phase

  1. Acute ureteric obstruction.
  2. Acute pyelonephritis—may be unilateral or bilateral.
  3. Renal vein thrombosis.
  4. Traumatic renal contusion


Bilateral striated nephrogram

  1. Acute pyelonephritis—may be asymmetrical.
  2. Abnormal renal tubules—e.g. acute tubular necrosis, acute
    interstitial nephritis, tubular protein deposition (rhabdomyolysis,
    HIV nephropathy).
  3. Hypotension/shock*.Adrenals, urinary tract, testes and prostate 263
  4. Medullary sponge kidney—in the medulla only. Parallel or
    fan-shaped streaks radiating from the papilla to the
    corticomedullary junction (‘paintbrush’ appearance), representing
    dilated contrast-filled tubules. Nephrocalcinosis often also present.
  5. Autosomal recessive polycystic kidney disease*—contrast
    medium in dilated tubules

Spotted nephrogram

  1. Vasculitis—e.g. polyarteritis nodosa, Wegener’s granulomatosis,
    SLE, drug-induced. Causes multiple infarcts of differing ages due to
    occlusion of small intrarenal arteries.
  2. Multiple emboli—usually from a cardiac source.
  3. Pyelonephritis—less common than a striated nephrogram

Reverse rim nephrogram


Bilateral nonenhancing renal cortices with enhancement of the
medulla and renal capsule. Pathognomonic for acute cortical
necrosis, most commonly due to pregnancy-related complications
(e.g. placental abruption, infected abortion, preeclampsia). Other
causes include shock, sepsis, trauma, hyperacute transplant
rejection, HUS, sickle cell disease, NSAIDs.


Typically reflects haemosiderin deposition in the renal cortex due
to intravascular haemolysis, resulting in low T1 and T2 signal

  1. Paroxysmal nocturnal haemoglobinuria—most common cause.
  2. Mechanical haemolysis—caused by malfunctioning prosthetic
    heart valves.
  3. Severe sickle cell disease*—although haemolysis is predominantly
    extravascular (causing haemosiderin deposition in the liver, spleen
    and bone marrow), intravascular haemolysis can also occur in
    severe crises.264 Aids to Radiological Differential Diagnosis
  4. Renal cortical necrosis—cortical thinning and low signal due to
    diffuse calcification.

Necrosis of the renal papilla in the medulla due to interstitial
nephritis or ischaemia. Involved kidneys are small with smooth
outlines in chronic disease, or large in acute fulminant cases

  1. Bilateral—in 85% multiple papillae are affected. Diabetes (50%),
    analgesics and sickle cell disease are the most important causes;
    others include trauma, acute tubular necrosis, shock (in infants)
    and chronic alcoholism.
  2. Unilateral—usually due to obstruction, renal vein thrombosis,
    acute pyelonephritis or TB.
  3. Papillae may show:
    (a) Enlargement (early) due to oedema. On CT, early disease
    presents as ill-defined areas of hypoenhancement in the
    papillary regions on the nephrographic phase. On US,
    echogenic rings may be seen in the medulla surrounded
    by a rim of fluid.
    (b) Partial sloughing—fissuring of the papilla occurs in one of two
    (i) Central (medullary type)—a contrast-filled fissure forms at
    the tip of the papilla ± a central cavity (‘ball-on-tee’ or
    ‘egg-in-cup’ sign on excretory phase).
    (ii) Forniceal (papillary type)—fissuring occurs at the edges of
    the papilla causing a ‘lobster claw’ appearance—if this
    progresses it leads to total sloughing.
    (c) Total sloughing (signet ring sign)—the sloughed papillary
    tissue may:
    (i) Fragment and be passed in the urine.
    (ii) Cause ureteric obstruction.
    (iii) Remain free in a calyx as a filling defect (echogenic on US).
    (iv) Remain in the pelvis and form a ball calculus.
    (d) Necrosis in situ—the papilla is shrunken and necrotic but has
    not separated. This may then become calcified or ossified
    (particularly in analgesic nephropathy and TB).
  4. Calyces—will appear dilated and clubbed following total sloughing
    of a papilla. On US this presents as a cystic cavity in the medulla
    contiguous with the calyces.



  1. Renal artery stenosis—see Section 9.25. Note that other arterial
    abnormalities such as aneurysms and AVMs can also rarely cause
    renovascular hypertension.
  2. Chronic bilateral parenchymal disease—e.g. glomerulonephritis,
    polycystic disease, diabetic glomerulosclerosis, connective tissue
    diseases (SLE, scleroderma, PAN), analgesic nephropathy.
  3. Chronic reflux nephropathy or obstructive uropathy.
  4. Tumours producing renin—characteristic in juxtaglomerular cell
    tumours (rare, seen in young adults), but can also occur with
    Wilms tumours and RCC.
  5. Chronic renal infection—e.g. XGP, TB.
  6. Renal vein thrombosis.
  7. Radiotherapy.


  1. Direct signs—seen at the site of narrowing.
    (a) Peak systolic velocity (PSV) in main renal artery >200 cm/s.
    Correlates well with >60% stenosis.
    (b) Renal artery PSV ÷ aortic PSV >3.5 correlates with >60%
    (c) Turbulent flow in the poststenotic main renal artery.266 Aids to Radiological Differential Diagnosis
    (d) Lack of Doppler flow within main renal artery (indicates
  2. Indirect signs—seen distal to the site of narrowing. Less reliable
    than direct signs.
    (a) Tardus-parvus intrarenal waveform—blunted and delayed
    systolic upstroke, demonstrated by loss of the early systolic
    peak, a systolic upstroke gradient <3 m/s2
    and acceleration
    time >0.07 s (time from onset of systole to peak systole). High
    specificity but low sensitivity.
    (b) Intrarenal arterial resistive index >0.8.
    (c) Smooth renal atrophy



  1. Atherosclerosis—in ~75%, most commonly men >50 years.
    Bilateral in 30%. Stenosis of the proximal 2 cm of the renal artery
    is typical (± calcification); less frequently the distal artery or early
    branches at bifurcations.
  2. Fibromuscular dysplasia—in ~20%, typically women <50 years.
    Nonatherosclerotic noninflammatory vasculopathy resulting in
    mural fibroplasia. Bilateral in 60%. Multiple stenoses ± dilatations,
    which may give the characteristic ‘string of beads’ appearance.
    Most commonly affects the middistal renal artery ± hilar branches,
    but can also involve carotid, vertebral and mesenteric arteries.
  3. Renal artery dissection—usually due to extension of aortic
    dissection into the renal arteries, but can also occur due to trauma,
    instrumentation or spontaneously related to fibromuscular
    dysplasia, connective tissue disorders (Marfan and Ehlers-Danlos
    syndromes), severe atherosclerosis, malignant hypertension and
    extreme physical exertion. On imaging the dissection flap may be
    hard to visualize due to the small vessel size. Renal artery occlusion
    may also occur due to thrombosis or embolism.
  4. Arteritis—PAN typically causes multiple intrarenal artery
    microaneurysms ± stenoses ± renal infarcts of different ages. SLE,
    Wegener’s granulomatosis and drug-induced vasculitis can cause a
    similar appearance. Takayasu arteritis can cause stenosis
    of the proximal renal artery. Other rare causes include radiation
    vasculopathy, thromboangiitis obliterans, syphilis and congenital
  5. Renal artery entrapment—extrinsic compression of the renal
    artery by the diaphragmatic crus, due to an anomalous high
    origin of the renal artery. Usually presents in young patients.
  6. Neurofibromatosis*—can rarely cause long tapered stenoses of
    the middistal renal arteries, usually seen in patients <50 years.
  7. Midaortic syndrome—rare, seen in young patients. Causes long
    smooth narrowing of the suprarenal aorta ± renal artery
    involvement.Adrenals, urinary tract, testes and prostate 267
  8. Extrinsic compression—by tumour, lymph nodes, aneurysm
    or RPF



  1. Technical factors—incomplete filling during excretory
  2. Tumour—most commonly RCC (adult) or Wilms tumour (child).
  3. Obstructed infundibulum—due to tumour, calculus or TB.
  4. Duplex kidney—with a nonfunctioning upper or lower moiety.
    Signs suggesting a nonfunctioning upper moiety are:
    (a) Fewer calyces than the contralateral kidney. This sign is only
    reliable in unilateral duplication. (Calyceal distribution is
    symmetrical in 80% of normal individuals.)
    (b) A shortened upper calyx that does not reach into the upper
    pole and may be deformed by a dilated upper pole pelvis.
    (c) The kidney may be displaced downward or laterally by a
    dilated upper moiety pelvis. The appearances mimic a
    space-occupying lesion in the upper pole.
    (d) The upper pole may be rotated laterally and downward by a
    dilated upper moiety pelvis resulting in a ‘drooping lily’
    appearance of the lower pole calyces.
    (e) The lower moiety ureter may be displaced or compressed
    by the upper pole ureter, resulting in a series of scalloped
    (f) The lower moiety renal pelvis may be displaced laterally and
    its ureter then takes a direct oblique course to the lumbosacral
  5. Infection—abscess or TB.
  6. Partial nephrectomy—± a surgical defect in the twelfth rib

Extrinsic with a smooth margin 3

  1. Renal sinus masses—especially parapelvic and peripelvic cysts and
    benign mesenchymal tumours. These can indent and distort the pelvicalyceal system.
  2. Vascular impression—intrarenal arteries can produce transverse or oblique compression lines, most commonly indenting an upper pole calyx ± calyceal obstruction (Fraley syndrome). Collateral vessels can also cause impressions, e.g. ureteric artery collaterals in RAS (indenting the renal pelvis) and venous collaterals in IVC obstruction or gonadal vein varices (indenting the ureter).
    Renovascular AVMs can also indent the renal pelvis.
  3. Renal sinus lipomatosis—most commonly in older patients with chronic UTI or stones. Fat in the renal hilum produces a relative lucency on IVU and narrows and elongates the major calyces.

Arising from the wall with smooth margins

  1. Early urothelial carcinoma—in practice any urothelial mass lesion
    is considered malignant until proven otherwise, due to the overlap
    in imaging findings.
  2. Papilloma—most common benign ureteric tumour, can be solitary
    or multiple. Smooth surface, most commonly in distal ureter.
    Indistinguishable from early TCC and rare benign neoplasms, e.g.
    nephrogenic adenoma (caused by chronic inflammation),
    leiomyoma, neurofibroma, haemangioma, solitary fibrous tumour.
  3. Pyeloureteritis cystica—due to chronic infection. Multiple
    2–4-mm well-defined round submucosal cysts project into the
    lumen of the renal pelvis and/or ureter (upper > lower).
  4. Metastases—rare, usually in the presence of disseminated disease.
    Lung, breast and GI sources are the most common.
  5. Suburothelial haemorrhage—usually associated with
    coagulopathy or anticoagulants. Causes diffuse mural thickening ±
    filling defects in the renal pelvis and upper ureter. The thickening
    is hyperattenuating on unenhanced CT and does not usually cause
    significant obstruction, which can aid differentiation from TCC.
  6. Endometriosis*—stricturing is more common but filling defects
    can occur, typically in the distal ureter.
  7. Pseudodiverticulosis—multiple, usually bilateral, small (<5 mm)
    outpouchings from the upper-mid ureters. Associated with chronic
    UTI and obstruction, increased risk of malignancy.
  8. Stevens-Johnson syndrome—can cause multiple small mucosal
    bullae in both ureters with mucosal sloughing, which may cause Adrenals, urinary tract, testes and prostate 269
    obstruction. On CT there may be diffuse urothelial enhancement.
    Diagnosis usually already known due to cutaneous features.

Arising from the wall with an irregular margin

  1. Urothelial carcinoma—most common in the distal ureter, often
    multifocal. Enhances on CT.
  2. Squamous cell carcinoma—rare, strongly associated with chronic
    UTI and stones.
  3. Renal cell carcinoma—infiltrative subtypes may invade the
    pelvicalyceal system.
  4. Squamous metaplasia—associated with chronic infection or
    calculi. Most common in the bladder and renal pelvis.
    Premalignant lesion, indistinguishable from tumour.
  5. Tuberculosis*—causes nodular wall thickening and strictures.
  6. Malakoplakia—granulomatous reaction to chronic E. coli infection;
    causes single or multiple urothelial plaques, nodules or masses
    indistinguishable from malignancy.
  7. Amyloidosis*—can cause focal urothelial thickening and irregular
    filling defects ± calcification (highly suggestive).
  8. Sarcoidosis*—can rarely cause a ureteric filling defect (granuloma)

In the lumen

  1. Calculus.
  2. Blood clot—due to trauma, tumour or bleeding diathesis.
    May be adherent to the wall or free in the lumen.
    Hyperattenuating on unenhanced CT. Changes in size or
    shape over several days.
  3. Air bubble—see Section 9.38.
  4. Sloughed papilla—due to papillary necrosis. Often triangular,
    may be rim-calcified. Look for blunted papillae in kidney.
  5. Benign fibroepithelial polyp—rare, usually in the renal pelvis or
    ureter in young adults. Elongated, smooth and pedunculated—the
    stalk may be long, so the polyp can mimic an intraluminal lesion
    and may protrude into the bladder. Enhances on CT.
  6. Fungus ball—typically in the renal pelvis, due to aspergillosis or
    candidiasis in immunocompromised patients



  1. Pyelosinus backflow—contrast extravasation from fornix rupture
    into the renal sinus ± perinephric space. Contrast may also track
    inferiorly alongside ureter.
  2. Pyelotubular backflow—physiological reflux of contrast from the
    calyx into the terminal portions of collecting ducts in the renal
    papilla (not due to forniceal rupture). Fan-like streaks from a calyx
    into the medullary pyramid.
  3. Pyelointerstitial backflow—forniceal rupture into the renal
    interstitium; contrast flows from a calyx into the medullary
    pyramid ± renal cortex. More amorphous than pyelotubular.
  4. Pyelolymphatic backflow—forniceal rupture into renal sinus
    lymphatics; contrast flows into small serpiginous lymphatic
    channels extending medially towards paraaortic lymphatics.
  5. Pyelovenous backflow—forniceal rupture into arcuate or
    interlobar veins, with contrast flowing into the renal vein.

Dilated calyx with a narrow
infundibulum/renal pelvis

  1. Stricture—due to tumour, calculus or TB.
  2. Xanthogranulomatous pyelonephritis—typically there is a large
    calculus in a contracted and thickened renal pelvis, with gross
    calyceal dilatation and parenchymal atrophy.
  3. Infiltrative processes of the renal sinus—these can constrict the
    renal pelvis and cause calyceal dilatation (see Section 9.19).Adrenals, urinary tract, testes and prostate 271
  4. Extrinsic compression by an artery—most commonly a right
    upper pole calyx (Fraley syndrome). The renal pelvis is normal.
  5. Calyceal diverticulum (mimic)—congenital outpouching that
    communicates with a calyceal fornix via a thin isthmus. May
    contain milk of calcium or dependent calculi (highly suggestive of
    a diverticulum).

Dilated calyx with a wide infundibulum and normal
renal pelvis

  1. Chronic reflux or obstruction—generally all the calyces are
    affected + associated parenchymal atrophy. The renal pelvis may
    be mildly dilated.
  2. Papillary necrosis—clubbed calyces due to sloughing of papillae.
    See Section 9.23.
  3. Congenital megacalyces—dilated and clubbed calyces (due to
    hypoplasia of medullary pyramids) usually with a normal renal
    pelvis. Number of calyces is often increased (polycalycosis) up to
    20–25 (normal 8–12). Normal cortical thickness and good renal
    function differentiate it from chronic reflux/obstruction.

Dilated calyces and renal pelvis with a normal ureter

  1. Congenital PUJ obstruction—due to abnormal embryogenesis of
    the PUJ resulting in a variable degree of stenosis. Often presents in
    childhood (or detected antenatally), but can present in adults.
    Extrinsic crossing vessels at the PUJ may contribute to obstruction.
  2. Acquired PUJ obstruction—due to malignant and benign
    strictures, calculus (and other filling defects), previous trauma or
  3. Peripelvic cysts (mimic)—can be hard to differentiate from
    hydronephrosis on US. Excretory phase CT is diagnostic.


In the wall

  1. Oedema or stricture due to calculus—the calculus may have passed.
  2. Primary tumour—TCC, papilloma and other benign and
    malignant neoplasms (see Section 9.27).
  3. Metastasis—can present as a thick-walled stricture. Usually in the
    presence of disseminated disease. Lung, breast and GI sources are
    the most common.
  4. Postsurgical—e.g. a misplaced ligature, following ureteric
    instrumentation or at a ureteral anastomosis.
  5. Tuberculous stricture—typically multifocal stricturing causing a
    beaded or corkscrew ureter ± calcification. A particular hazard
    during the early weeks of treatment.
  6. Schistosomiasis*—chronic disease causes distal ureteric
    stricturing ± calcification in the ureter or bladder
  7. Ureterocoele—cystic dilatation of the ureter at the VUJ, projects
    into bladder. Due to congenital stenosis at ureteric orifice.
    Commonly associated with ectopic ureteric insertion (e.g. in
    duplex systems). Beware of a pseudoureterocoele due to an
    obstructing stone or mass at the VUJ.
  8. Radiation ureteritis.
  9. Malakoplakia—causes mural nodules and masses ± obstruction.
  10. Amyloidosis*—can cause a ureteral stricture ± calcification
    (highly suggestive).
  11. Vasculitis—e.g. PAN, Wegener’s granulomatosis, HSP, ChurgStrauss syndrome. Can rarely cause single or multiple ureteric
  12. Primary obstructive megaureter—dilated pelvicalyceal system
    and ureter (>6 mm) transitioning to a normal calibre aperistaltic
    distal ureter, without a visible obstructing lesion. Congenital,
    often diagnosed antenatally but can present at any age.
  13. Congenital midureteric stricture—short smooth stenosis in the
    midureter. Presents in infancy or antenatally, but is often
    mistaken for PUJ obstruction or megaureter


Outside the wall 6

  1. Retroperitoneal fibrosis—tethers and obstructs the midureters + medial deviation. Other infiltrative retroperitoneal processes can also obstruct the ureters but tend not to cause deviation, e.g. amyloidosis, Erdheim-Chester disease and extramedullary haematopoiesis.
  2. Direct invasion of the ureter from pelvic and retroperitoneal malignancies—e.g. cervix, endometrium, bladder, prostate, rectum, lymphoma.
  3. Stricture due to adjacent inflammation—e.g. appendicitis, diverticulitis, Crohn’s disease, tuboovarian abscess, pelvic actinomycosis, inflammatory AAA.
  4. Endometriosis*—typically causes distal ureteric stricturing + other features on MRI.
  5. Extrinsic compression from benign pelvic masses—e.g. large uterine fibroids, pelvic lipomatosis.
  6. Retrocaval ureter—right side only. Dilated upper ureter with a transition to normal as the ureter courses medially behind IVC


No obstruction or reflux


Vesicoureteric reflux
Dilated pelvicalyceal system and ureter down to the VUJ (as
opposed to primary megaureter where the distal ureter is of
normal calibre) + demonstrable reflux. The ureter may become
very dilated and tortuous. See Section 14.61.
No obstruction or reflux
1. Pregnancy—in the third trimester, R>L side.
2. Residual dilatation following relief of obstruction—most
commonly following passage of a ureteric calculus or post
3. Polyuria or diuresis—e.g. medication, diabetes insipidus.
4. Urinary tract infection—due to the effect of P-fimbriated E. coli
on the urothelium.
5. Primary nonobstructive megaureter—similar to primary
obstructive megaureter except there is usually no



Medial deviation

  1. Normal variant—in 15%, due to large iliopsoas muscles displacing
    distal ureters medially.
  2. Retroperitoneal fibrosis—medially displaced midureters. See
    Section 9.33.
  3. Retrocaval ureter—the right ureter passes behind the IVC at the
    level of L4. The distal ureter lies medial to the dilated proximal
  4. Pelvic lipomatosis—nearly always in men, most common in
    Afro-Caribbeans. Medial displacement of the distal ureters with
    elevation and elongation of the bladder (‘pear-shaped’) and
    rectum + widened presacral space. Lucent on plain film, CT shows
    diffuse symmetrical fatty proliferation around bladder and rectum. 274 Aids to Radiological Differential Diagnosis
    May cause ureteric obstruction and cystitis glandularis. Chronic
    proctitis (e.g. due to UC or radiotherapy) can cause a similar
    appearance but the fatty proliferation is limited to the mesorectal
  5. Following abdominoperineal resection—the distal ureters are
    medially placed.
  6. Pelvic sidewall mass—e.g. haematoma, lymphadenopathy, iliac
    artery aneurysm. Medially displaces one or both distal ureters

Lateral deviation
Much more common than medial deviation.

  1. Hypertrophy of psoas muscles—can displace upper ureters laterally.
  2. Retroperitoneal mass—e.g. lymphadenopathy, haematoma,
    abscess, lymphocoele, sarcoma, neurogenic tumours. Displaces
    upper ureters.
  3. Pelvic mass—e.g. fibroids, ovarian tumour. Displaces distal ureters.
  4. Aneurysmal aortic dilatation—displaces upper ureters.
  5. Postoperative—e.g. urostomy, ureterolysis.
  6. Prune-belly syndrome



  1. Lymphoma*—most common. Confluent mass or masses of
    paraaortic/iliac lymph nodes, typically homogeneous and mildly
    enhancing on CT. Infiltrative, tends to surround vessels without
    causing significant narrowing. Often lifts the aorta away from the
    spine (‘floating aorta’ sign). Necrosis is rare except in very
    high-grade lymphomas. Calcification is rare except post
  2. Other causes of retroperitoneal lymphadenopathy.
    (a) Metastases—common sources include kidneys, cervix,
    prostate and testes. Central necrosis, if present, aids
    differentiation from lymphoma. Extranodal retroperitoneal
    metastases can also rarely be seen, e.g. from lung cancer or
    melanoma, usually in the presence of metastatic disease
    elsewhere.Adrenals, urinary tract, testes and prostate 275
    (b) Infection—e.g. TB or MAC. Nodes are typically necrotic.
    Most common in immunocompromised patients.
    (c) Sarcoidosis—most commonly involves periportal nodes in
    the abdomen but paraaortic nodes can also be involved.
    Usually homogeneous, <2 cm and discrete (in contrast
    to the confluent adenopathy seen in lymphoma).
    (d) Castleman disease—benign lymph node hyperplasia.
    Presents as single or multiple avidly enhancing lymph node
    masses in the peripancreatic, paraaortic or iliac regions ±
    intratumoural vessels. Often homogeneous, may be
    heterogeneous if large ± calcification.
    (e) Rosai-Dorfman disease
    —can rarely cause retroperitoneal
    adenopathy or masses.
  3. Nonneoplastic masses and infiltrative disorders
    (a) Vascular malformations—retroperitoneal collateral veins are
    commonly seen in portal hypertension. IVC anomalies are
    occasionally seen (e.g. left-sided, double, azygos
    continuation). Congenital AVMs are rare, usually seen in the
    pelvis. Haemangiomas are very rare in the retroperitoneum
    but may show characteristic marked T2 hyperintensity on
    MRI ± peripheral or progressive enhancement. Phleboliths
    and peripheral interdigitating fat may also be seen.
    (b) Retroperitoneal fibrosis—see Section 9.33.
    (c) Erdheim-Chester disease—characteristic rind of soft tissue
    around the aorta and kidneys. T1/T2 hypointense, minimal
    (d) Extramedullary haematopoiesis—well-defined,
    heterogeneous soft-tissue masses ± fat, in a paravertebral or
    presacral location. Splenomegaly and diffuse skeletal changes
    (sclerosis in myelofibrosis, expansion in thalassaemia) are
    usually also present indicating bone marrow failure.
    (e) Amyloidosis
    —infiltrative, poorly enhancing, soft-tissue mass
    or thickening that may be focal or diffuse throughout the
    retroperitoneum ± involvement of mesentery and omentum.
    T2 hypointense on MRI. Often contains characteristic coarse
    (f) Old rejected renal transplant—located in the right or left
    iliac fossa. Atrophic and poorly enhancing with areas of
    calcification, may mimic a tumour. Surgical clips and vascular
    anastomoses are indicative.
  4. Sarcomas—many different types (most common are below).
    Often large, well-defined ± invasion of adjacent structures. Note
    that rhabdomyosarcoma is the most common sarcoma in
    children (very rare in adults).
    (a) Liposarcoma—most are characteristically fatty, but
    pleomorphic variants contain little or no fat, presenting as a
    nonspecific heterogeneously enhancing soft-tissue mass. 276 Aids to Radiological Differential Diagnosis
    Myxoid variants appear pseudocystic due to low attenuation
    on CT and high T2 signal on MRI, but internal reticular
    enhancement aids differentiation from true cysts.
    (b) Leiomyosarcoma—often shows extensive necrosis and cystic
    change. Intravascular extension, e.g. into the IVC, is a
    characteristic feature if present (although angiosarcoma can
    also do this). Calcification is rare. F>M.
    (c) Undifferentiated pleomorphic sarcoma—nonspecific
    heterogeneously enhancing mass. Calcification is not
    uncommon, and necrosis is usually less extensive than in
    leiomyosarcoma. M>F.
  5. Neurogenic tumours—often occur in younger adults cf.
    sarcomas. Typically well-defined and usually benign but
    malignant varieties/transformation can occur.
    (a) Schwannoma—round/oval encapsulated mass, can be
    homogeneous (if small) or heterogeneous with areas of cystic
    degeneration and calcification (if large or ‘ancient’). Variable
    enhancement. Located along peripheral nerves, most
    commonly paravertebral ± nodular extension along the
    course of the nerve or towards a neural foramen.
    (b) Neurofibroma—round or plexiform in shape, located along
    peripheral nerves. Low attenuation on CT (20–25 HU) with
    only mild enhancement. On MRI the target sign is
    characteristic if present: peripheral T2 hyperintensity (myxoid
    component) + central T2 hypointensity (cellular component).
    Extension into a spinal neural foramen is also characteristic.
    Plexiform neurofibromas are diagnostic of NF1 and present
    as fusiform expansion of peripheral nerves, usually bilateral
    and symmetrical (most commonly involving the lumbosacral
    plexus). These are at higher risk of malignant transformation:
    significant asymmetry, progressive enlargement, irregular
    infiltrative margins, areas of necrosis or perilesional oedema
    are worrying features.
    (c) Paraganglioma—most common extraadrenal location is
    paraaortic distal to the inferior mesenteric artery origin
    (organs of Zuckerkandl). Typically shows avid enhancement
    on CT and MRI ± flow voids. May be homogeneously T2
    bright or heterogeneous due to haemorrhage, necrosis and
    calcification. Uptake on MIBG scintigraphy is diagnostic.
    Typical clinical features (e.g. hypertension) may be present.
    Associated with NF1, MEN-2 and vHL. Risk of retroperitoneal
    haemorrhage. Up to 40% are malignant (large size and
    irregular margins are worrying features).
    (d) Ganglioneuroma—benign tumour arising from paravertebral
    sympathetic ganglia. Well-defined and lobulated, often
    extending around vessels without causing significant
    narrowing. May extend into neural foramina. Adrenals, urinary tract, testes and prostate 277
    Homogeneously hypoattenuating on unenhanced CT
    (myxoid stroma) ± calcification. Heterogeneously T2
    hyperintense on MRI ± characteristic whorled appearance.
    Heterogeneous delayed enhancement. Necrosis is rare. The
    more malignant ganglion cell tumours (neuroblastoma and
    ganglioneuroblastoma) nearly always occur in children.
  6. Germ cell tumour—nearly always in men. Large lobulated
    paraaortic mass; homogeneous if seminoma, heterogeneous with
    haemorrhage and necrosis if nonseminomatous. Calcification and
    fat suggests teratoma (F>M). Most represent metastatic disease
    from a testicular primary, but the primary tumour may ‘burn
    out’, leaving only a testicular scar and a paraaortic mass—this
    tends to be ipsilateral to the primary testicular tumour, whereas
    primary retroperitoneal germ cell tumours tend to be centred on
    the midline. Elevated serum αFP or ß-HCG can aid differentiation
    from other heterogeneous tumours.
  7. Desmoid tumour—benign but locally aggressive, with a high
    rate of recurrence. Heterogeneously enhancing infiltrative mass,
    may be T2 hyperintense (cellular) or hypointense (fibrotic). Often
    invades the abdominal wall, may encase and narrow vessels.
    Associated with Gardner variant FAP.
  8. Solitary fibrous tumour—well-defined, lobulated, usually benign.
    Typically shows marked heterogeneous enhancement ±
    intratumoural vessels—these features are suggestive but can also
    be seen in paraganglioma (characteristic location ± clinical
    features), angiosarcoma (usually ill-defined ± intravascular
    extension) and Castleman disease (often more homogeneous).
    Cystic change, necrosis or haemorrhage can occur. Calcification is
  9. Undescended testis ± tumour—located along the expected
    course of testicular descent, most commonly close to the deep
    inguinal ring. Associated gonadal vessels and absence of the
    testis within the scrotum are pathognomonic. Increased risk of
    tumour development, usually presents when large.
  10. Leiomyoma—rare, nearly always in women (often with a history
    of uterine leiomyomas); usually located in the pelvis. T2
    hypointense on MRI ± areas of cystic change (particularly if large)
    ± intratumoural vessels (angioleiomyoma). May mimic
  11. Primary sex cord stromal tumour—very rare, seen only in
    women (usually peri- or postmenopausal). Usually in the pelvis
    (broad ligament) but can rarely be higher in the retroperitoneum.
    Nonspecific, heterogeneous mass ± calcification. An elevated
    oestrogen level is suggestive.
  12. Perivascular epithelioid cell tumour (PEComa)—very rare, usually
    in middle-aged women. Most are benign. Nonspecific, well-defined,
    heterogeneously enhancing mass.278 Aids to Radiological Differential Diagnosis
  13. Extragastrointestinal stromal tumour—very rare. Nonspecific,
    well-defined, heterogeneously enhancing mass ± calcification.
  14. Extramedullary plasmacytoma—very rare, most commonly
    perinephric in location. Nonspecific, infiltrative mass on imaging



  1. Nonneoplastic cystic lesions—most common.
    (a) Pseudocyst—typically forms after an episode of acute
    pancreatitis; has a thick, enhancing wall and often
    heterogeneous contents ± foci of fat. Usually located close to
    the pancreas. A nonpancreatic pseudocyst can also rarely
    occur, representing a nonresolving, chronic haematoma.
    (b) Urinoma—occurs after rupture of the renal collecting system
    or bladder. Thin-walled, unilocular, located adjacent to the
    rupture site. May fill with contrast on delayed postcontrast
    images if there is an ongoing urine leak.
    (c) Lymphocoele—occurs after retroperitoneal
    lymphadenectomy due to leakage of lymph from cut
    lymphatics (look for surgical clips). Thin-walled, unilocular,
    located adjacent to iliac vessels or aorta. Fluid may have
    negative HU value on CT due to fat content.
    (d) Haematoma—most commonly due to coagulopathy; other
    causes include trauma and bleeding aneurysms or tumours
    (particularly AML and paraganglioma). Heterogeneous
    high attenuation on CT ± active contrast extravasation; if
    fluid–fluid levels are present (‘haematocrit’ sign) this indicates
    as the cause.
    (e) Abscess—enhancing wall, heterogeneous contents ± gas.
    Clinical features of sepsis. Common locations include
    perinephric, within psoas muscle and paravertebral (consider
    discitis). (a) to (d) can also become infected and resemble an
    abscess. If the abscess has a well-defined wall with minimal
    surrounding oedema/fat stranding, consider TB (cold
  2. Lymphangioma—congenital malformation; can present at any
    age, more common in men (cf. items 3-8 below). Often large
    and elongated, characteristically traversing different
    compartments. Thin-walled, usually multilocular with no
    enhancement. May contain fat density/signal due to lymph.
    Calcification is rare except in lymphangiomatosis (multiple
    widespread lymphangiomas).
  3. Cystadenoma—almost exclusively in women, can be mucinous
    or serous. Thin-walled unilocular cyst, usually in a lateral location.
    Solid nodules indicate malignant transformation to
    cystadenocarcinoma.Adrenals, urinary tract, testes and prostate 279
  4. Epidermoid cyst—usually in the presacral space in middle-aged
    women, but can rarely be higher in the retroperitoneal space.
    Thin-walled, unilocular, typically near the midline.
  5. Müllerian cyst—only occurs in women, typically obese with
    menstrual irregularity. Thin-walled, uni- or multilocular, usually in
    a lateral location.
  6. Cystic mesothelioma—benign, most common in middle-aged
    women. Usually arises from the pelvic peritoneum but can rarely
    be retroperitoneal. Thin-walled, multilocular.
  7. Cystic teratoma—benign, typically occurs in young girls.
    Complex cystic mass + characteristic foci of calcification
    and fat.
  8. Lymphangioleiomyoma—cystic mass or masses with peripheral
    enhancement ± chylous ascites. Arises from lymphatics in the
    paraaortic region or next to iliac vessels. Only occurs in women
    with lymphangioleiomyomatosis, so look for the characteristic
    lung cysts.
  9. Bronchogenic cyst—usually mediastinal, but can rarely be in the
    subphrenic retroperitoneal space. Thin-walled, unilocular,
    nonenhancing ± mural calcification. May be hyperattenuating
    due to proteinaceous contents.
  10. Dilated cisterna chyli—located to the right of the aorta in the
    retrocrural space. Tubular, continues cranially as the thoracic
  11. Cystic change in a solid neoplasm—some solid tumours (such
    as paragangliomas, schwannomas, leiomyomas, leiomyosarcomas
    and synovial sarcomas) can show marked cystic change,
    becoming predominantly cystic with a thick irregular enhancing
    wall. Note that myxoid tumours appear pseudocystic, but the
    reticular internal enhancement (best seen on MRI) helps
    distinguish these from true cystic lesions.
  12. Hydatid cyst—rare. Encapsulated, multilocular, no internal


Fat containing

  1. Liposarcoma—usually large and unencapsulated, displaces and
    compresses the adjacent kidney. Contains a mixture of fat and
    soft tissue ± calcification. Amount of fat is variable:
    well-differentiated tumours are usually almost entirely fatty +
    thick fibrous septa; dedifferentiated tumours are fatty with
    nodular soft-tissue components >1 cm or foci of calcification;
    myxoid and pleomorphic variants contain little or no fat.
  2. Angiomyolipoma—typically arises from the kidney but can be
    very exophytic or rarely completely extrarenal, mimicking a
    liposarcoma. Prominent intratumoural vessels or aneurysms and
    an associated cortical notch in the adjacent kidney indicate AML.280 Aids to Radiological Differential Diagnosis
  3. Retroperitoneal fat necrosis—usually due to severe acute
    pancreatitis. Initially presents as ill-defined fat stranding, evolving
    into multiple fat-containing soft-tissue nodules, which involute
    over time. Can also involve mesenteric and omental fat.
    Long-term steroids can also cause fat necrosis but are more
    localized. Trauma or surgery can cause encapsulated fat necrosis:
    a thick, enhancing capsule and internal fat–fluid level are
  4. Perinephric lipomatosis—usually due to chronic infection or
    stones. Diffuse unencapsulated fatty proliferation with no
    soft-tissue components. A similar appearance can be seen with
    antiretroviral-associated lipodystrophy in patients with HIV.
  5. Lipoma—rare in the retroperitoneum. Even a purely fatty
    retroperitoneal mass should be treated as suspicious for a
    well-differentiated liposarcoma.
  6. Teratoma—rare, typically in young patients. Mature teratomas
    are encapsulated and contain a mixture of fat, soft tissue
    and calcification; a fat–fluid level is characteristic. Malignant
    teratomas usually contain little fat, and in men most represent
    metastases from a testicular primary (which may have
    ‘burned out’).
  7. Hibernoma—rare, benign tumour of brown fat. Slightly higher
    attenuation than normal fat on CT (and slightly lower T1 signal
    on MRI) with internal septa ± enhancement. A prominent feeding
    vessel is almost pathognomonic. Typically shows high FDG
    uptake on PET (cf. well-differentiated liposarcomas, which show
    low grade uptake).
  8. Extraadrenal myelolipoma—usually presacral, but can rarely
    arise higher in the retroperitoneum. Encapsulated fatty mass with
    streaky soft-tissue components. Can mimic liposarcoma but
    appears more well-defined and shows uptake on sulfur colloid
  9. Extramedullary haematopoiesis—haematopoietically inactive
    areas (yellow marrow) contain fat.
  10. Others—paragangliomas, ganglioneuromas, haemangiomas and
    lymphangiomas can rarely contain macroscopic fat.
    Lipoblastomas appear similar to liposarcomas but occur only in
    infants and children.


  1. Dense retroperitoneal/periaortic fibrotic soft-tissue mass
    (hypoechoic on US) that typically begins around the aortic
    bifurcation and extends superiorly to the renal arteries. Can rarely
    extend into the mesenteric root or into the pelvis. Reactive
    retroperitoneal lymphadenopathy is not uncommon.
  2. Encases the aorta (usually sparing its posterior aspect and not
    displacing it away from the spine) and IVC, lymphatics and ureters
    ± obstruction. The ureters are tethered by the fibrosis and deviated
  3. In the acute inflammatory phase the mass shows moderate
    enhancement, T2 hyperintensity on MRI and uptake on PET. In the
    chronic fibrotic phase the mass shows minimal enhancement, T2
    hypointensity and no uptake on PET.

Secondary 7

  1. Primary (‘idiopathic’)—>70%. Most cases now found to be
    autoimmune, due to IgG4-related disease. Similar histologically to
    chronic periaortitis and inflammatory AAA.
  2. Secondary
    (a) Retroperitoneal malignancy—lymphoma and some metastases (e.g. from breast, stomach, colon, kidney, bladder, prostate, cervix, carcinoid, sarcomas) can trigger a desmoplastic reaction similar to RPF; lymphadenopathy tends to be more pronounced and metastases may be seen elsewhere. Malignancy often displaces the aorta away from the spine and may invade the psoas muscles or spine. Soft-tissue extension or adenopathy above the renal arteries is also suggestive of malignancy.
    (b) Retroperitoneal haemorrhage—e.g. due to ruptured aneurysm, trauma, surgery, coagulopathy. Blood incites a fibrotic reaction similar to RPF.
    (c) Inflammatory conditions—e.g. Crohn’s, diverticulitis, TB, histoplasmosis, actinomycosis, pyelonephritis and extravasation of urine.
    (d) Connective tissue diseases—e.g. ankylosing spondylitis, SLE, rheumatoid arthritis, PAN, Wegener’s granulomatosis, Churg-Strauss syndrome, sarcoidosis.
    (e) Other infiltrative retroperitoneal processes—particularly
    Erdheim-Chester disease, which characteristically causes a soft-tissue rind around the aorta (+ involvement of its posterior margin) and kidneys, usually sparing the ureters. Amyloidosis can also infiltrate the retroperitoneum but appears more diffuse than RPF, and does not usually involve the ureters.
    (f) Drugs—e.g. ergot derivatives, dopamine agonists, hydralazine,
    ß-blockers, analgesics.
    (g) Retroperitoneal radiotherapy

Within the lumen

  1. Calculus.
  2. Foreign body—e.g. catheter, ureteric stent and other self-inserted
    objects. If chronic these can become encrusted with calcification.
  3. Blood clot—hyperattenuating on unenhanced CT, no acoustic
    shadow on US, no vascularity or enhancement. If serpiginous in
    appearance, suggests bleed from upper urinary tract.
  4. Ureterocoele—cystic dilatation of ureter projecting into the
    bladder at VUJ or ectopic insertion site, giving a ‘cobra-head’
    appearance on IVU.
  5. Fungus ball—in immunocompromised patients, due to candidiasis
    or aspergillosis
Arising from the wall
malignant 8
Benign 6
Inflammatory 5
\+ 3
  1. Malignant neoplasms—much more common than benign neoplasms. In practice all bladder polyps or masses are presumed malignant until proven otherwise, as imaging features overlap widely.
    (a) Urothelial carcinoma—accounts for 90% of bladder tumours in adults. Presents as a polypoid or papillary mass projecting into the lumen, or as an area of focal wall thickening and/or enhancement. Often multifocal, tends to recur. Invades perivesical fat ± adjacent organs in advanced cases. May have calcification along its surface.
    (b) Squamous cell carcinoma—<5% of bladder tumours, but >50% in areas where schistosomiasis is endemic. Other risk factors are chronic UTI and bladder calculi. Usually sessile and locally invasive, but otherwise indistinguishable from TCC.
    (c) Adenocarcinoma—<2% of bladder tumours, classically associated with a persistent urachus or bladder exstrophy. Presents as a focal mass/polyp or, in the signet ring variant, as diffuse bladder wall thickening (like linitis plastica).
    (d) Metastasis—most commonly from RCC, melanoma, breast or stomach.
    (e) Sarcoma—rare in adults, but rhabdomyosarcoma is the most common bladder tumour in children. Leiomyosarcoma is the most common bladder sarcoma in adults, usually large and invasive with areas of necrosis.
    (f) Lymphoma*—rare, secondary > primary. Usually a discrete nonspecific mass.
    (g) Neuroendocrine tumours—e.g. carcinoid tumour (small, polypoid) and small cell carcinoma (large, highly invasive and aggressive). Rare.
    (h) Melanoma—rare, may be T1 hyperintense on MRI. Can also arise in urethra.
  2. Benign neoplasms.
    (a) Papilloma—usually small but essentially indistinguishable from papillary TCC.
    (b) Leiomyoma—submucosal in location, smooth and well-defined with homogeneous low T2 signal on MRI ± cystic areas. Can be hard to differentiate from well-differentiated leiomyosarcoma on imaging.
    (c) Neurofibroma—rare. Low attenuation on CT, T2 hyperintense on MRI + central hypointensity. May be focal, or diffuse/plexiform in NF1.
    (d) Paraganglioma—rare. Avidly enhancing mass ± ring calcification ± characteristic history of micturition-induced hypertension and headache.
    (e) Haemangioma—rare; small, hypervascular, homogeneously T2 bright.
    (f) Solitary fibrous tumour—rare; large, well-defined, heterogeneous enhancement.
  3. Inflammatory lesions.
    (a) Nephrogenic adenoma—metaplastic response to chronic infection, stones, trauma or surgery. Usually solitary, can be polypoid or sessile. Does not invade muscularis or perivesical fat. Not premalignant, but often recurs.
    (b) Cystitis cystica and glandularis—metaplastic response to chronic infection, obstruction or stones, differentiating into either cystic lesions (cystica) or mucin-secreting glands (glandularis)—both often coexist. Cystitis cystica presents as multiple small submucosal cysts. Cystitis glandularis can
    present as an enhancing polypoid mass. Does not invade muscularis or perivesical fat.
    (c) Malakoplakia—uncommon chronic inflammatory response to E. coli infection, most often seen in the bladder. Variable appearances—solitary or multiple, polypoid or plaque-like, small or large, homogeneously or heterogeneously enhancing, intraluminal or invading perivesical fat. Indistinguishable from malignancy.
    (d) Inflammatory pseudotumour—rare, most often seen in young adults. Single heterogeneously enhancing mass, may invade perivesical fat.
    (e) Eosinophilic cystitis—rare. May present as diffuse bladder wall
    thickening or as a focal nonspecific enhancing mass.
  4. Infection—TB and schistosomiasis.
  5. Amyloidosis*—rare, but the bladder is the most common involved
    site in the urinary tract. Usually causes focal bladder wall thickening or mass ± characteristic mural calcification.
  6. Ectopic prostate—rare congenital anomaly. Small intramural
    nodule usually in the trigone or urethra


  1. Prostatic enlargement—median lobe often protrudes into the
    bladder base in benign prostatic hyperplasia (BPH).
  2. Pelvic lymphadenopathy, mass or collection—indents bladder
    outline. Pelvic malignancies (e.g. prostate, cervix, rectum) may also
    directly invade the bladder.
  3. Enlarged uterus—e.g. fibroids, pregnancy. Indents bladder dome.
  4. Inflammation adjacent to the bladder—e.g. Crohn’s disease,
    diverticulitis. Causes focal bladder wall thickening adjacent to the
    inflammatory process. Intravesical gas suggests a fistula.
  5. Iliac artery aneurysm—look for curvilinear calcification on XR.
  6. Colonic distension.
  7. Urachal cyst or mass—may indent the bladder dome in the
  8. Endometriosis*—most often seen on the serosal surface of the
    posterior bladder wall in the uterovesical pouch. Deposits can
    grow through the bladder wall and create filling defects. Typically
    T1 hyperintense on MRI due to haemorrhage + enhancement +
    other sites of involvement in the pelvis.



  1. Any cause of cystitis—e.g. infection, haemorrhagic cystitis (e.g.
    due to radiation or chemotherapy—look for intraluminal blood
    clots), trauma, eosinophilic cystitis, interstitial cystitis.
  2. Tuberculosis*—diffuse bladder wall thickening ± irregular mucosal
    masses in the acute phase. Contracted thick-walled bladder ±
    calcification in the chronic phase. Nearly always secondary to renal
    involvement, so the presence of normal kidneys practically
    excludes TB.
  3. Schistosomiasis*—diffuse nodular bladder wall thickening in the
    acute phase, similar to TB except that infection starts in the
    bladder and progresses up the urinary tract. Diffuse bladder wall
    calcification ± contraction/fibrosis in the chronic phase.
  4. Malakoplakia—can involve the bladder circumferentially


Muscular hypertrophy

  1. Chronic bladder outlet obstruction—e.g. due to BPH, urethral
    stricture, posterior urethral valves. Bladder is typically distended.
  2. Neurogenic bladder (upper motor neuron damage only)—
    characteristic ‘pine cone’ appearance on cystogram in severe cases
    due to elongated and trabeculated bladder, which may be
    distended or small. Note that lower motor neuron damage and
    sensory neuropathy both lead to a distended, thin-walled bladder.



  1. Signet-ring adenocarcinoma—‘linitis plastica’ appearance.
  2. Metastases—from gastric cancer or leukaemia.
  3. Lymphoma*—rare; 10% present as diffuse bladder wall
  4. Plexiform neurofibroma—can diffusely involve the bladder wall.
    Low attenuation on CT, T2 hyperintense on MRI + central
    hypointensity. Rare; diagnostic of NF1


In the lumen

  1. Calculus—may have passed through the ureter (typically <5 mm)
    or grown within the bladder (often large, round, may be
    laminated or spiculated).
  2. Foreign body—encrustation of a ureteric stent or catheter
  3. Tumour—e.g. TCC, SCC, paraganglioma, inflammatory
    pseudotumour. Typically surface calcification, so looks intraluminal
    on unenhanced CT (may be the only sign of an underlying
  4. Alkaline-encrusted cystitis—due to Corynebacterium infection.
    Results in encrustation along infected urothelium. Can involve
    bladder or upper tracts


In the wall

  1. Schistosomiasis*—infrequent in the Western hemisphere but the
    most common cause of mural calcification worldwide. Thin
    curvilinear calcification outlining a bladder of (usually) normal size
    and shape. Calcification spreads to the distal ureters in 15%.
  2. Tuberculosis*—rare and usually accompanied by calcification
    elsewhere in the urogenital tract. Contracted fibrotic bladder.
  3. Chronic radiation or chemotherapy-induced cystitis—e.g.
    cyclophosphamide and mitomycin C. Contracted thick-walled
    bladder that can rarely calcify.
  4. Tumour—mucinous adenocarcinoma may contain fine punctate
    calcification. Haemangioma may contain phleboliths.
  5. Amyloidosis*—rare. Can cause focal bladder wall calcification



1. Bladder exstrophy—extruded bladder communicating with skin
surface (surgically corrected in infancy). Markedly widened pubic
symphysis on plain film (manta ray sign).
2. Imperforate anus—high type. Rectum can fistulate with bladder
or urethra.
3. Patent urachus—bladder communicates with umbilicus.
1. Diverticular disease—most common cause.
2. Crohn’s disease.
3. Appendix abscess—and other pelvic sepsis.
4. Tuberculosis
1. Carcinoma of the colon, bladder or reproductive organs.
2. Radiotherapy—usually 12–18 months after treatment.
1. Accidental.
2. Iatrogenic—particularly in obstetrics and gynaecology
(vesicovaginal fistula).



Gas in the bladder lumen

  1. Following instrumentation—e.g. catheterization or cystoscopy.
  2. Vesicointestinal fistula—diverticular disease, Crohn’s disease and
    carcinoma of the colon or rectum.
  3. Cystitis—due to gas-forming organisms and fermentation,
    especially in diabetics. Usually E. coli. Clostridial infections are rare,
    and usually secondary to septicaemia.
  4. Penetrating wounds


Gas in the bladder wall

  1. Emphysematous cystitis—usually in diabetics

Gas in the ureters and pelvicalyceal systems

  1. Any cause of gas in the bladder.
  2. Ureteric diversion—into the colon or bladder.
  3. Fistula—most commonly with colon or duodenum; other sites
    include stomach, small bowel, skin or vagina. Most commonly
    iatrogenic (e.g. nephrostomy, nephrolithotomy, hysterectomy);
    other causes include urinary calculi, XGP, TB, trauma, malignancy,
    radiotherapy, diverticulitis, Crohn’s disease or duodenal ulcer.
  4. Emphysematous pyelitis—usually in diabetics. Gas may also be
    present in the renal parenchyma (emphysematous pyelonephritis)
    ± retroperitoneum


  1. Congenital anomalies—due to incomplete involution. Any of
    these can be complicated by infection, stone formation or
    malignant transformation.
    (a) Patent urachus—the entire urachus remains patent, resulting
    in urine leaking from the umbilicus. Typically presents in
    (b) Urachal cyst—a focal portion of the urachus remains patent
    but does not communicate with the umbilicus or bladder,
    thereby forming a fluid-filled cyst. Unilocular with a thin
    minimally enhancing wall (unless infected).Adrenals, urinary tract, testes and prostate 289
    (c) Urachal sinus—the umbilical end of the urachus remains
    patent, resulting in a blind-ending sinus extending inferiorly
    from the umbilicus ± intermittent discharge.
    (d) Vesicourachal diverticulum—the bladder end of the urachus
    remains patent, resulting in a midline outpouching from the
    anterosuperior bladder dome.
  2. Infection—most common complication of urachal anomalies, most
    often by S. aureus and E. coli. Heterogeneous echogenicity on US,
    mural enhancement + surrounding fat stranding on CT. Can form
    an abscess ± fistula. May mimic urachal carcinoma if large and
  3. Malignancy—usually adenocarcinoma; most are mucinous with
    areas of calcification. Typically located adjacent to the bladder
    dome—a midline supravesical mass containing calcification is
    almost diagnostic of urachal carcinoma. Mucinous components
    will appear cystic on CT and T2 hyperintense on MRI. Solid
    components will enhance. Less common malignancies include
    TCC, SCC and sarcoma.
  4. Benign tumours—e.g. adenoma, cystadenoma, fibroma,
    fibroadenoma, fibromyoma, hamartoma. Very rare,
    indistinguishable from carcinoma.
  5. Mimics of urachal lesions.
    (a) At the umbilicus—an omphalomesenteric duct sinus can
    mimic an urachal sinus, although the former usually courses to
    the right (towards the distal ileum) rather than inferiorly in the
    midline. Other causes of periumbilical inflammation can mimic
    an infected urachal sinus.
    (b) Supravesical—other lesions inseparable from the bladder
    dome can mimic a urachal tumour or abscess, e.g.
    endometrioma, ovarian torsion, invasive bladder cancer,
    malakoplakia, inflammatory pseudotumour, peritoneal
    metastasis, appendiceal abscess, dropped gallstone

Seminal vesicles and vas deferens

  1. Diabetes mellitus—vast majority of cases. Bilateral and
    symmetrical linear calcification of the vas deferens wall. Ageing
    and secondary hyperparathyroidism can produce an identical
  2. Chronic infection—mainly TB but also schistosomiasis, chronic
    UTI, gonorrhoea and syphilis. Vas deferens calcification is
    intraluminal and usually unilateral or asymmetrical. Seminal vesicles
    can show wall calcification in chronic schistosomiasis.
  3. Seminal vesicle/ejaculatory duct calculi—rare, usually secondary
    to ejaculatory duct obstruction (e.g. congenital or due to chronic


  1. Benign calcification—typically located in the periurethral region or at the interface between transitional and peripheral zones. Most commonly due to chronic prostatitis (including TB and schistosomiasis) or BPH, but can also rarely be seen in hyperparathyroidism and may be extensive in alkaptonuria.
  2. Prostate cancer—calcification within the peripheral zone is suggestive of underlying malignancy.
  3. Impacted calculus in the prostatic urethra—located in the midline.
  4. Seed brachytherapy—multiple tiny radioactive seeds implanted for treatment of prostate cancer. Very dense on plain film and CT. Radiation therapy can also cause prostate calcification


  1. Testicular microlithiasis—multiple (>4) 1–3mm echogenic
    nonshadowing intratesticular foci, usually bilateral. Common
    incidental finding. No follow-up needed in low-risk asymptomatic
    patients. Note that solitary punctate calcification in an otherwise
    normal testis usually represents a phlebolith or sperm granuloma.
  2. Scrotal pearl—represents a previously torted and detached
    testicular or epididymal appendix. Often mobile, located between
    the layers of tunica vaginalis. The appendix may also calcify in situ
    without detaching.
  3. Previous trauma, torsion or infection—including TB. Calcification
    may be intratesticular or in the epididymis or tunica albuginea ± a
    chronic haematocoele or pyocoele. Missed torsion leads to an
    atrophic testis containing multifocal calcification.
  4. Calcification in a mass lesion—Sertoli cell tumours and
    nonseminomatous germ cell tumours often contain calcification,
    especially those with a teratoma component. A ‘burned-out’
    testicular tumour can regress into an irregular focus of calcification.
    Calcification can also be seen in the walls of cysts and
    epidermoids, and within paratesticular fibrous pseudotumours.
  5. Sperm/suture granuloma—occurs at vasectomy site on vas
  6. End-stage renal failure—can produce bilateral epididymal


  1. Peyronie’s disease—the fibrous plaques on the tunica albuginea
    can calcify.
  2. End-stage renal failure—can cause calcification of vessels or
    tunica albuginea in the penis.



  1. Benign prostatic hyperplasia—most common prostatic mass.
    Presents as well-defined nodular enlargement of the transitional
    zone with heterogeneous T2 signal on MRI. May protrude into the
    bladder base.
  2. Prostatic adenocarcinoma—95% of prostate cancers. 70% arise
    from the peripheral zone (in contrast to BPH). T2 hypointense on
    MRI + restricted diffusion + early enhancement and washout. Easier
    to detect in the peripheral zone (which is normally T2
    hyperintense) than the transitional zone, where it can be hard to
    differentiate from BPH nodules—ill-defined margins, lentiform
    shape, homogeneous T2 hypointensity + restricted diffusion
    favours carcinoma. Tumours may show extracapsular invasion ±
    involvement of seminal vesicles, bladder, rectum or pelvic floor/
    sidewall. Typically metastasizes to lymph nodes and bones
    (sclerotic deposits), and less commonly to lung and liver.
  3. Benign mimics of prostate cancer
    (a) Postbiopsy haemorrhage—commonly seen in the peripheral
    zone, usually resolves after 6–8 weeks. Causes T2 hypointensity
    ± restricted diffusion, but the presence of T1 hyperintensity
    distinguishes this from cancer.
    (b) Prostatitis—acute, chronic and granulomatous (e.g. TB,
    malakoplakia, sarcoidosis) prostatitis all usually involve the
    peripheral zone, causing focal or diffuse T2 hypointensity +
    restricted diffusion indistinguishable from cancer.
    Granulomatous prostatitis can also extend beyond the
    prostate. Prostatitis can lead to necrosis and atrophy of the
    peripheral zone resulting in volume loss, T2 hypointensity and 292 Aids to Radiological Differential Diagnosis
    restricted diffusion. Volume loss and low-level enhancement
    can help differentiate this from carcinoma.
    (c) Normal structures—the anterior fibromuscular stroma
    (anterior to transitional zone) and central zone (around
    ejaculatory ducts) are both homogeneously and symmetrically
    T2 hypointense and must not be mistaken for carcinoma.
  4. Secondary malignancy—usually due to direct prostate invasion
    from bladder or rectal cancer. Tumours of the prostatic urethra
    (e.g. carcinoma, melanoma) can also invade the prostate.
    Metastases (e.g. from lung, melanoma, GI tract) are less
  5. Rare prostate neoplasms—serum prostate specific antigen (PSA)
    is usually normal. Bone metastases, if present, are usually lytic (in
    contrast to the sclerotic metastases seen in adenocarcinoma).
    (a) Other carcinomas—SCC, TCC and BCC can rarely arise from
    the prostate. SCC is T2 hypointense, indistinguishable from
    adenocarcinoma. TCC and BCC may be T2 hyperintense. SCC
    and TCC have a poor prognosis.
    (b) Sarcomas—most common are rhabdomyosarcoma (in
    children) and leiomyosarcoma (in adults). Usually much larger
    than adenocarcinoma and more heterogeneous on T2 and
    postcontrast sequences due to haemorrhage and necrosis.
    Often invades adjacent structures and metastasizes early.
    (c) Stromal tumour of uncertain malignant potential
    (STUMP)—well-defined heterogeneously enhancing
    solid-cystic mass, often large. Involves both peripheral and
    transitional zones (in contrast to BPH, which displaces the
    peripheral zone). May be adherent to rectum, often recurs
    after surgery. Can transform into stromal sarcoma.
    (d) Lymphoma*—homogeneous soft-tissue mass, which can
    involve the whole prostate. Usually secondary involvement,
    with disease present elsewhere.
    (e) Neuroendocrine tumours—e.g. carcinoid (low grade,
    heterogeneously T2 hyperintense), small cell carcinoma (high
    grade, very aggressive), paraganglioma (T2 hyperintense, avid
    enhancement, characteristic clinical picture of headache,
    tachycardia and sweating induced by micturition or rectal
  6. Rare benign lesions—e.g. inflammatory pseudotumour, solitary
    fibrous tumour, leiomyoma, neurofibroma, haemangioma, dermoid
  7. Amyloidosis*—rare; T2 hypointense with no restricted diffusion
    and minimal enhancement



  1. Midline—(a)-(c) are located posterior to the prostatic urethra and
    are unilocular and T2 bright on MRI, with variable T1 signal
    depending on protein content. Infection and stone formation can
    (a) Utricle cyst—small (8–10 mm), does not extend beyond
    prostate. Communicates with prostatic urethra. May be
    associated with other congenital genitourinary anomalies.
    (b) Müllerian duct cyst—larger, elongated, usually extends above
    the prostate. Does not communicate with urethra.
    (c) Ejaculatory duct cyst—rare, due to obstruction and dilatation
    of ejaculatory duct. Usually small and paramedian, may appear
    in the midline if large. Can communicate with urethra, vas
    deferens and/or seminal vesicles.
    (d) Cowper’s duct cyst (mimic)—located inferior to the prostatic
    apex within the urogenital diaphragm or bulb of the corpus
    spongiosum. Usually unilocular, midline or paramedian. If
    large, may appear inseparable from the prostate. Usually
    communicates with the bulbous urethra.
    (e) TURP defect (mimic)—irregular periurethral urine-filled defect
    continuous with bladder lumen.
  2. Lateral
    (a) Cystic degeneration of BPH—most common cystic lesion.
    Occurs in the transitional zone only. Usually small and
    multiple, may contain haemorrhage or calculi.
    (b) Retention cyst—also occurs in BPH but can be located in any
    (c) Abscess—clinical features of acute prostatitis are key. Increased
    risk in diabetic or immunocompromised men. Irregular
    enhancing walls, heterogeneous contents ± septations +
    restricted diffusion. May rupture into urethra (creating a
    urethral pseudodiverticulum) or fistulate with the rectum. A
    tuberculous abscess may create multiple fistulae to the
    perineal and scrotal skin (‘watering can’ perineum).
    (d) Cavitary prostatitis—due to chronic prostatitis, resulting in
    cystic change throughout the gland (‘Swiss cheese’
    (e) Cystic tumours.
    (i) Cystic prostate carcinoma—some variants of
    adenocarcinoma (e.g. mucinous or ductal) can show
    cystic change. Usually located in the peripheral zone (in
    contrast to cystic BPH).
    (ii) Multilocular cystadenoma—benign cystic tumour with
    multiple enhancing septations, typically very large and
    extending well above the prostate without invasion of
    adjacent structures. May contain haemorrhage and small
    enhancing solid elements. Often appears in the midline
    due to its large size.
    (iii) Lymphangioma—rare. Multiloculated, minimal
    (f) Hydatid cyst—very rare. Encapsulated, multilocular, no
    internal enhancement


  1. Congenital—often associated with other genitourinary tract
    (a) Agenesis/hypoplasia—bilateral agenesis is associated with
    cystic fibrosis. Unilateral agenesis is often associated with
    ipsilateral renal agenesis.
    (b) Cyst—bilateral cysts are associated with ADPKD. A unilateral
    cyst (or cystic dilatation) is often associated with ejaculatory
    duct obstruction and ipsilateral renal agenesis—the triad of
    Zinner syndrome. The cyst may contain proteinaceous material
    (T1 hyperintense). A ureteric remnant is often present and may
    insert ectopically onto the cystic seminal vesicle or other sites.
  2. Secondary tumour invasion—most commonly by prostate cancer
    (stage T3b disease), less commonly by bladder or rectal cancer.
    The vas deferens may also be involved.
  3. Iatrogenic changes—prostate biopsy can cause seminal vesicle
    haemorrhage (intraluminal T1 hyperintensity helps differentiate this
    from malignant infiltration). Radiotherapy often causes bilateral
    symmetrical seminal vesicle atrophy with luminal narrowing or
    obliteration and diffuse mural T2 hypointensity.
  4. Infection—usually secondary to prostatitis (e.g. bacterial,
    tuberculous, schistosomiasis). Diffuse mural thickening and
    enhancement with luminal dilatation in the acute phase. An
    abscess may form, particularly in diabetics or following
    instrumentation. In chronic or recurrent infection the seminal
    vesicles atrophy.Adrenals, urinary tract, testes and prostate 295
  5. Amyloidosis*—common in the elderly. Bilateral diffuse T2
    hypointense mural thickening and luminal narrowing. The lack of
    restricted diffusion or enhancement helps distinguish this from
    malignant infiltration.
  6. Primary seminal vesicle tumours—very rare. Malignant tumours
    (infiltrative appearance) are more common and include
    adenocarcinoma, sarcoma and seminoma. Benign tumours
    (well-defined) include cystadenoma (multiloculated cystic mass),
    leiomyoma, fibroma, schwannoma, paraganglioma, dermoid cyst.
  7. Hydatid cyst—very rare. Multiloculated with nonenhancing septa


  1. Germ cell tumours—95% of testicular tumours in young men,
    nearly always unilateral. Usually hypervascular on US. Risk factors
    include undescended testes (even if corrected), previous
    contralateral germ cell tumour or positive family history. The
    primary tumour may ‘burn out’, regressing into an irregular focus
    of calcification, but any metastases will remain.
    (a) Seminoma—~50%. Typically a solid well-defined
    homogeneously hypoechoic mass contained within the testis.
    May be multifocal. Necrosis and calcification are rare. 25%
    have retroperitoneal nodal disease at presentation. αFP and
    ß-HCG are usually normal.
    (b) Nonseminomatous germ cell tumour—usually contains a
    mixture of embryonal, teratoma, yolk sac and choriocarcinoma
    components. More aggressive than seminoma and more
    heterogeneous due to necrosis, haemorrhage, cystic change
    and calcification. Often invades tunica albuginea. αFP, ß-HCG
    and LDH often raised. Pure yolk sac tumour is the most
    common testicular tumour in children.
    (c) Epidermoid cyst—most common benign testicular tumour.
    Characteristic ‘onion skin’ appearance on US: well-defined
    avascular mass containing concentric echogenic rings of 296 Aids to Radiological Differential Diagnosis
    keratin. Alternatively may be hypoechoic with a central
    echogenic focus (target appearance). May be rim-calcified.
  2. Sex cord stromal tumours—usually benign but indistinguishable
    from malignancy on imaging; usually small, solitary, hypoechoic
    and hypervascular. Leydig cell tumours are the most common and
    may secrete testosterone or oestrogen. Sertoli cell tumours can
    calcify, may secrete oestrogen and are associated with
    Peutz-Jeghers syndrome and Carney complex. Rarer subtypes
    include granulosa cell tumour and thecoma-fibroma.
  3. Lymphoma*—most common testicular malignancy in men >60
    years, usually secondary. Hypoechoic and hypervascular on US,
    often multifocal and bilateral. May be diffuse. Leukaemia can look
  4. Metastases—rare, usually in patients >50 years. May be bilateral.
    Most common sources include prostate, lung, kidney, colon and
  5. Cystadenoma of the rete testis—rare. Multiloculated cystic
    tumour arising from rete testis. Has mass effect and may extend
    beyond testis (in contrast to tubular ectasia). Indistinguishable
    from cystadenocarcinoma therefore needs excision.
  6. Other rare tumours not limited to the testis—e.g.
    haemangioma, leiomyoma, lipoma, sarcoma, plasmacytoma,
    carcinoid tumour, neurofibroma. Apart from lipoma (well-defined
    and hyperechoic), these do not have specific imaging findings

Nonneoplastic cysts 3

  1. Tubular ectasia of the rete testis—geographic cluster of
    numerous small cysts replacing the mediastinum testis. No mass
    effect or Doppler flow. Often bilateral, more common in older
  2. Simple cyst—2–20 mm; unilocular, anechoic with an
    imperceptible wall. Usually solitary and often located near the
  3. Intratesticular varicocoele (mimic)—serpiginous with venous flow
    on Doppler

Usually painful

  1. Testicular torsion
    (a) Acute—presentation <24 hours. Enlarged isoechoic (early),
    hypoechoic or heterogeneous (late) testis ± hydrocoele and
    epididymal enlargement. Colour Doppler: absent testicular
    flow (complete torsion) or reduced diastolic arterial flow Adrenals, urinary tract, testes and prostate 297
    (partial torsion <360 degrees); normal peritesticular flow. A
    twist in the spermatic cord may be seen (most specific sign).
    (b) Subacute or missed—presentation at 1–10 days. Hypoechoic
    heterogeneous testis due to infarction. Colour Doppler: absent
    testicular flow; increased peritesticular flow. Testis atrophies in
    the chronic phase.
    (c) Spontaneous detorsion—colour Doppler: normal or increased
    testicular flow; increased peritesticular flow.
  2. Segmental infarction—due to infection, trauma, transient torsion,
    vasculitis (most commonly PAN), sickle cell disease or
    hypercoagulable states. Geographic hypoechoic hypovascular area
    extending to periphery of testis


  1. Epididymoorchitis—generalized testicular and/or epididymal
    swelling and hypoechogenicity initially; progresses to patchy focal
    low reflectivity. Hypoechoic areas are hypervascular. Isolated
    orchitis is rare except in mumps. Complications occur in 50%—
    abscess, necrosis, haematoma and testicular atrophy/scarring.
  2. Abscess—complicating epididymoorchitis, often in diabetics or
    those with mumps. Hypoechoic (or mixed) with an irregular
    ill-defined wall and low level internal echoes. No internal
    vascularity, but peripheral hyperaemia is often seen.
  3. Granulomatous infection—e.g. TB, brucellosis, syphilis,
    schistosomiasis, leprosy and fungal infections. Presentation is
    usually subacute, and pain is less marked. US appearances vary,
    ranging from diffuse epididymoorchitis to a focal abscess or mass
    mimicking malignancy. In TB and schistosomiasis, other sites of
    urinary tract involvement are usually present. TB may also create a
    sinus tract to the scrotal skin. Other infections tend to occur in
    immunocompromised patients


  1. Testicular haematoma—hypoechoic and avascular. History of
    trauma is indicative.
  2. Testicular sarcoidosis—typically presents in Afro-Caribbean men
    (in whom testicular cancer is rare) with multiple bilateral small
    painless hypoechoic masses in the testes and epididymides. Usually
    occurs in the presence of multisystem involvement.
  3. Testicular lipomatosis—multiple, usually bilateral, small
    well-defined hyperechoic lesions. No mass effect or
    hypervascularity. Pathognomonic for Cowden syndrome.
  4. Testicular adrenal rests—seen in congenital adrenal hyperplasia.
    Variable echogenicity; usually multiple, bilateral and located next
    to mediastinum testis.
  5. Other rare disorders not limited to the testis—e.g. malakoplakia,
    amyloidosis, Rosai-Dorfman disease. Nonspecific testicular mass
    indistinguishable from malignancy.

Within epididymis

  1. Epididymitis—acute history of pain. Enlarged, hypoechoic,
    hypervascular epididymis with a hydrocoele and skin thickening ±
    involvement of testis (epididymoorchitis). May be complicated by
    an epididymal abscess: complex cystic lesion with an irregular wall,
    no internal vascularity with surrounding hyperaemia. Consider
    granulomatous infection (e.g. TB) if presentation is subacute.
  2. Spermatocoele—unilocular or multilocular cyst in epididymal head
    containing low level echoes (‘falling snow’) representing
  3. Epididymal cyst—unilocular simple cyst in any part of epididymis,
    no internal echoes.
  4. Postvasectomy ectasia—epididymis enlarges and appears
    heterogeneous due to obstruction and dilatation of epididymal
    ducts. A sperm granuloma may also be seen.
  5. Sarcoidosis*—epididymal enlargement or focal hypoechoic
    nodules. More common than testicular involvement. Usually
    bilateral, in the presence of disease elsewhere.
  6. Neoplasms—most are benign.
    (a) Adenomatoid tumour—most common, benign. Well-defined,
    solid, hypovascular, often hyperechoic on US, most common
    in the tail.
    (b) Leiomyoma—well-defined hypoechoic mass ± cystic change,
    usually in the head.
    (c) Papillary cystadenoma—benign. Typically a mixed solid-cystic
    mass in the head. Associated with vHL (especially if bilateral).Adrenals, urinary tract, testes and prostate 299
    (d) Lymphoma*/leukaemia—rare, often bilateral. Testicular
    involvement is more common and more extensive (in contrast
    to sarcoidosis and TB).
    (e) Metastasis—e.g. from prostate, kidney, GI tract, pancreas. Rare.
    (f) Other rare tumours—e.g. lymphangioma (multiloculated
    cystic mass), haemangioma, neurofibroma, sarcoma,
    adenocarcinoma and plasmacytoma.
  7. Epididymal filariasis—parasites can be seen moving within dilated
    epididymal lymphatics on US (‘filarial dance sign’). Endemic in
    tropical areas.


  1. Hydrocoele—serous fluid collection between layers of tunica
    vaginalis. Can be congenital (due to patent processus vaginalis) or
    reactive to scrotal infection, torsion or malignancy. Envelops the
    testis (cf. large epididymal cysts which displace the testis).
  2. Pyocoele/haematocoele—due to infection (pyocoele) or trauma/
    surgery (haematocoele). Complex paratesticular fluid collection
    with internal echoes and septations, ± gas if pyocoele.
  3. Tunica albuginea cyst—2–5 mm, unilocular or septated, located
    on the surface of the testis.
  4. Scrotal pearl—see Section 9.40.
  5. Fibrous pseudotumour—benign reactive fibrous proliferation,
    typically arises from tunica vaginalis. Single or multiple hypoechoic
    hypovascular masses ± calcification ± hydrocoele.
  6. Other rare benign tumours of the tunica vaginalis—e.g.
    adenomatoid tumour, leiomyoma (can also arise from dartos
    muscle), lipoma, solitary fibrous tumour.
  7. Malignancies of peritoneal origin involving the tunica
    (a) Metastasis—disseminated peritoneal malignancy + a patent
    processus vaginalis allows spread of tumour (and fluid) into
    the tunica vaginalis.
    (b) Mesothelioma—typically in older men with a history of
    asbestos exposure. Usually presents as multiple masses or
    nodules on the tunica vaginalis + hydrocoele. Benign variants
    can also occur in younger men.
    (c) Ovarian-type epithelial tumours—histologically identical to
    ovarian surface epithelial tumours and primary peritoneal
    carcinoma. Usually mixed solid-cystic.
  8. Supernumerary testis—isoechoic to, and smaller than, the
    adjacent normal testis.
  9. Splenogonadal fusion—ectopic splenic tissue attached to the
    testis (nearly always the left; may be undescended).
    Homogeneously hypoechoic on US, may have a prominent feeding
    vessel ± a band of splenic/fibrous tissue connecting the testis to
    the spleen

Related to spermatic cord

  1. Varicocoele—dilated pampiniform plexus of veins >2 mm on US.
    Seen in 15% of adult men, usually on the left side. Important to
    exclude a retroperitoneal mass, particularly in the older patient, if
    bilateral or if the history is short.
  2. Inguinoscrotal hernia—protrudes from the inguinal canal into the
    scrotum, enlarges with Valsalva.
  3. Lipoma—most common extratesticular nonepididymal tumour.
    May mimic a hernia but is separate from the deep inguinal ring
    and does not enlarge with Valsalva. Well-defined, avascular, usually
    uniformly hyperechoic.
  4. Hydrocoele of the spermatic cord—may be encysted (resembling
    a simple cyst) or may communicate with peritoneal space via a
    patent processus vaginalis (funicular type).
  5. Sperm granuloma—occurs following vasectomy at the cut ends of
    the vas deferens. Well-defined hypoechoic mass.
  6. Spermatic cord haematoma—most commonly following inguinal
    hernia repair but can also occur due to trauma, ruptured
    varicocoele or anticoagulation.
  7. Leiomyoma—usually in the inguinal part of the spermatic cord (in
    contrast to leiomyosarcoma, which is usually in the scrotal part).
  8. Sarcoma—most common spermatic cord malignancy, most often
    rhabdomyosarcoma (teenagers and children), liposarcoma or
    leiomyosarcoma (older men). These present as large
    heterogeneous invasive soft-tissue masses, apart from
    well-differentiated liposarcomas, which are mostly fatty and
    well-defined (albeit difficult to characterize on US).
  9. Other rare tumours—e.g. adenomatoid tumour, aggressive
    angiomyxoma, cellular angiofibroma, haemangioma, nerve sheath
    tumours, paraganglioma, rhabdomyoma, dermoid cyst,
    lymphoma, plasmacytoma.


  1. Trauma—typically short in length, developing weeks or months
    after the trauma. Straddle injuries cause strictures of the bulbous
    urethra. High-energy pelvic fractures cause strictures of the
    membranous urethra. Iatrogenic trauma, e.g. instrumentation and
    prostatectomy, causes strictures of the bulbomembranous and
    prostatic urethra respectively.
  2. Infection—usually due to chronic or recurrent gonococcal
    urethritis. Strictures are usually long/multiple and irregular, most
    commonly in the bulbous urethra, and may be complicated by a
    periurethral abscess ± perineal or scrotal fistula. Small contrast-filled
    outpouchings (periurethral glands) strongly suggest infection.
    Urethral TB is rare but causes strictures of the anterior urethra with
    multiple perineal and scrotal fistulae (‘watering can’ perineum).
  3. Urethral cancer—usually SCC (anterior urethra) or TCC (prostatic
    urethra), but adenocarcinoma and rarely leiomyosarcoma,
    melanoma and lymphoma can also occur. Most arise from the
    bulbomembranous urethra and present as a palpable mass ±
    urinary obstruction or bleeding. An irregular urethral stricture or
    change in morphology of a previously benign stricture suggests
    malignancy. MRI shows a T2 hypointense mass and aids local
  4. Secondary urethral malignancy—rare. Bladder TCC can seed to
    the urethra. Direct invasion of the urethra can occur from
    prostatic, rectal and scrotal malignancies. Penile metastases (e.g.
    from prostate, melanoma, colon) can erode into the urethra.
  5. Balanitis xerotica obliterans—lichen sclerosus of the penis. Causes
    meatal stenosis ± strictures of the penile urethra.
  6. Congenital stricture—rare, usually presents in childhood.
  7. Benign urethral lesions—very rare, present as a filling defect
    rather than a stricture. Examples include papilloma, leiomyoma,
    haemangioma, fibroepithelial polyp (congenital, arises from
    verumontanum), malakoplakia, amyloidosis and condyloma
    acuminata (due to HPV infection; multiple papillary filling defects
    in anterior urethra + cutaneous papillomas on the penis)