RENAL Flashcards
CONGENITAL RENAL ANOMALIES
Anomalies of position
- 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
CONGENITAL RENAL ANOMALIES
Anomalies of form
- 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). - 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). - Pancake/discoid kidney—bilateral fused pelvic kidneys, usually
near the aortic bifurcation. - Renal hypoplasia—incomplete development results in a smaller
kidney (<50% of normal size) with fewer calyces and papillae.
Normal function
CONGENITAL RENAL ANOMALIES
Anomalies of number
- 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. - 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. - 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
LOCALIZED BULGE OF THE RENAL OUTLINE ON IVU
- Cyst—well-defined nephrographic defect with a thin wall on the
outer margin. Beak sign. Displacement and distortion of smooth-walled calyces without obliteration. - Tumour—mostly RCC in adults and Wilms tumour in children.
- Fetal lobulation—the lobule directly overlies a normal calyx. Normal interpapillary line.
- 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.
- Splenic impression—on the left side only, producing an apparent bulge inferiorly.
- 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. - Localized compensatory hypertrophy—e.g. adjacent to an area of pyelonephritic scarring.
- 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.
- 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.
- 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
UNILATERAL SCARRED KIDNEY
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- 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. - Tuberculous autonephrectomy (putty kidney)—calcification
differentiates it from the other members of this section. - Lobar infarction—a broad contour depression over a normal
calyx. Normal interpapillary line. - 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.
UNILATERAL SMALL SMOOTH 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
affected.
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
diabetes.
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.
BILATERAL SMALL SMOOTH KIDNEYS
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
UNILATERAL LARGE SMOOTH KIDNEY
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
nonenhancing.
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
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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
kidney.
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
bilateral).
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
BILATERAL LARGE SMOOTH KIDNEYS
Developmental
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.
Inflammation/oedema
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.
Miscellaneous
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
RENAL CALCIFICATION
Dystrophic calcification due to localized disease
- 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. - Tumours—e.g. RCC, Wilms tumour, TCC, metastasis.
- Cysts—rim/septal calcification, usually related to previous infection
or haemorrhage. Common in ADPKD. - Vascular—e.g. in a chronic perinephric haematoma, or curvilinear
calcification in atherosclerotic/aneurysmal renal arteries.
RENAL CALCULI Calcium oxalapte/phosphate 75% Pure ca oxalate Struvite 15% Cystine Uric acid Xanthine -RL
Calcium-containing
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
hypercalciuria.
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).
Struvite
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.
Cystine
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
include:
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).
Xanthine
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
- Protease inhibitors, e.g. Indinavir—used in HIV treatment. Most
common medication-induced calculus—other causes include
sulphonamides, ciprofloxacin, ephedrine, guaifenesin. - Matrix—mainly composed of mucoproteins. Tend to occur in
patients with a history of UTIs, renal stones or proteinuria on
dialysis
MIMICS OF RENAL COLIC ON
UNENHANCED CT UROGRAPHY
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.
Gynaecological
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.
Gastrointestinal
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
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Pancreatic and hepatobiliary disorders
1. Gallstones.
2. Pancreatitis and pancreatic tumours.
Vascular
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/
coagulopathy.
Musculoskeletal
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
NEPHROCALCINOSIS
Medullary (pyramidal)
- 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. - Hyperparathyroidism*—usually bilateral and symmetrical, diffuse
rather than punctate. - 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. - Renal papillary necrosis—calcification of necrotic papillae. Usually
asymmetrical. See Section 9.23. - Causes of hypercalcaemia or hypercalciuria—e.g. malignancy
(bone metastases, myeloma, paraneoplastic syndromes),
sarcoidosis, hypervitaminosis D, milk-alkali syndrome and
idiopathic hypercalciuria. - 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. - Hyperoxaluria—typically causes diffuse cortical and medullary
nephrocalcinosis as well as nephrolithiasis. Primary form presents in
childhood.
NEPHROCALCINOSIS Cortical 6 Mnem: COAGI GOATI
- Acute cortical necrosis—classically ‘tramline’ calcification, occurs
in the chronic phase. - Chronic glomerulonephritis—bilateral curvilinear or punctate
cortical calcification. - Chronic infection—multifocal nodular cortical calcification can
occur with HIV-related renal infections, e.g. Pneumocystis jirovecii,
Mycobacterium avium complex (MAC) and CMV. - Chronic renal transplant rejection—due to cortical necrosis.
- Hyperoxaluria—typically causes diffuse cortical and medullary
nephrocalcinosis. - 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 CYSTIC DISEASE
Renal dysplasia
- 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. - 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.
RENAL CYSTIC DISEASE
Polycystic kidney disease*
- 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. - 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
RENAL CYSTIC DISEASE
Cystic tumours
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- 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. - Multilocular cystic RCC—5% of RCCs are cystic (variant of clear
cell RCC). Nodular components on imaging suggest RCC. - 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. - Angiomyolipoma with epithelial cysts—rare cystic variant of
AML. Indistinguishable from cystic RCC on imaging. - Primary renal sarcoma—e.g. leiomyosarcoma, angiosarcoma. Rare
and aggressive, usually solid but can occasionally be predominantly
cystic with enhancing nodular components. - Cystic Wilms tumour—extremely rare in adults
RENAL CYSTIC DISEASE
Cortical cysts
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- 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).
- 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. - 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. - 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.
- 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
RENAL CYSTIC DISEASE
Medullary cysts
- 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. - 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. - Papillary necrosis—clubbed calyces may mimic cysts on US.
- 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.
RENAL CYSTIC DISEASE
Miscellaneous
- 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 - Traumatic—intrarenal haematoma or urinoma.
- Endometriosis*—renal involvement is rare, usually presents with a
complex haemorrhagic cystic lesion.
RENAL CYSTIC DISEASE
Extraparenchymal renal cysts
- 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. - 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
FAT-CONTAINING RENAL MASS
- 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. - 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. - 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. - Lipoma—rare. Composed entirely of fat, no soft-tissue component.
Similar on CT to a fat-rich AML. - Oncocytoma—can rarely contain a small focus of macroscopic fat.
- Xanthogranulomatous pyelonephritis—xanthomatous material
within dilated calyces can be of low attenuation on CT similar to
fat density. - Wilms tumour—very rare in adults.
- Teratoma—very rare, usually found in children or adolescents.
Contains varying amounts of soft tissue, fat and calcification. A
fat–fluid level is characteristic. - Renal sinus lipomatosis—expansion of the renal sinus fat without
a soft-tissue component, secondary to chronic inflammation
SOLID RENAL LESIONS
Well-defined mass
- 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. - 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. - 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
9 - 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. - 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. - 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. - 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
calcification. - 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. - 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). - 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
sarcoma. - 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. - 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
SOLID RENAL LESIONS
Infiltrative lesions
ill-defined, hypovascular and do not usually distort the
renal contour
- 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. - 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. - 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. - 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. - 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. - Leukaemia—typically causes bilateral diffuse renal enlargement
but can rarely present with single or multiple masses (chloroma
in acute myeloid leukaemia). - 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
9 - Sarcomas—rare. Angiosarcoma and rhabdomyosarcoma often
have an infiltrative growth pattern. - Other rare lesions—e.g. plasmacytoma, extramedullary
haematopoiesis, inflammatory pseudotumour, Wegener’s
granulomatosis, Rosai-Dorfman disease, amyloidosis. - 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.
RENAL SINUS MASS
Neoplastic
7
- 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
obstruction. - Squamous cell carcinoma—strongly associated with renal calculi
and chronic UTI. - Metastasis to sinus lymph nodes.
- Lymphoma*—may be limited to the renal sinus, particularly in
PTLD. Ill-defined hypovascular mass which characteristically does
not cause obstruction. - Mesenchymal tumour—e.g. lipoma, medullary fibroma,
haemangioma, leiomyoma. - Retroperitoneal tumours extending into the renal sinus—any
retroperitoneal tumour but lymphoma most commonly. - Renal parenchymal tumours projecting into the renal
sinus
RENAL SINUS MASS
Nonneoplastic lesions
- Peripelvic cyst—typically multiple and bilateral, arise from
lymphatics within sinus fat. See Section 9.15. - Parapelvic cyst—single, larger cyst protruding into the sinus,
originating from the adjacent parenchyma. See Section 9.15. - Sinus lipomatosis—echogenic central sinus complex on US. CT
and MRI directly reveal fatty nature. - Vascular—renal artery aneurysm, AVM or renal vein varix can
manifest as peripelvic lesions. Colour Doppler or contrast-enhanced
CT are diagnostic. - Inflammatory—soft-tissue thickening in the sinus due to chronic/
severe pyelonephritis, XGP or malakoplakia. - Haematoma—due to anticoagulants or less commonly trauma.
- Urinoma—due to pelvicalyceal rupture, usually associated with
ureteral obstruction (e.g. stones), PUJ obstruction or trauma
(including surgery). - 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
masses.
(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
9
(d) Amyloidosis*—can rarely involve the renal sinuses, causing
infiltrative soft-tissue masses which may calcify (highly
suggestive).
(e) Extramedullary haematopoiesis—look for signs of bone
marrow failure, e.g. bone sclerosis, splenomegaly. Uptake on
sulphur colloid scintigraphy is diagnostic.
NEOPLASTIC AND PROLIFERATIVE
DISORDERS OF THE PERINEPHRIC SPACE
Soft-tissue rind
- Lymphoma*—usually due to extension of renal/retroperitoneal
lymphoma into perinephric space, but can present as isolated
perinephric soft-tissue thickening. - Erdheim-Chester disease*—retroperitoneal involvement is
common and produces a characteristic rind of soft tissue around
the kidneys and aorta. - Amyloidosis*—may diffusely infiltrate the perinephric and
retroperitoneal fat ± foci of calcification (highly suggestive). - Retroperitoneal fibrosis—periaortic soft tissue may extend into
the perinephric space. - Metastases—most present as focal masses but breast cancer can
present as infiltrative retroperitoneal soft tissue, which can involve
the perinephric space. - Extramedullary haematopoiesis—can rarely infiltrate the
perinephric fat. - Rosai-Dorfman disease*—can rarely cause subcapsular renal
infiltration. - 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
NEOPLASTIC AND PROLIFERATIVE
DISORDERS OF THE PERINEPHRIC SPACE
Focal solid lesion
6
- Renal lesions extending into the perinephric space—e.g.
tumours (RCC, TCC), inflammatory lesions (malakoplakia, XGP). - 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.
- 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. - Nodular fat necrosis due to severe pancreatitis—usually presents with numerous small soft-tissue nodules (± central fat) throughout the intraabdominal fat.
- Primary sarcoma—some liposarcomas may present as a solid mass. Other sarcomas can also arise from the perinephric space.
- Other rare lesions not specific to the perinephric space—e.g.
haemangioma, solitary fibrous tumour, Castleman disease, desmoid tumour, inflammatory pseudotumour, plasmacytoma.
NEOPLASTIC AND PROLIFERATIVE
DISORDERS OF THE PERINEPHRIC SPACE
Fatty lesions
- 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. - 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. - Perinephric lipomatosis—associated with renal stones and chronic
renal infection (including XGP and TB). Expansion of the
perinephric and renal sinus fat ± stranding. - 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. - Extramedullary haematopoiesis—may contain foci of
macroscopic fat.
NEOPLASTIC AND PROLIFERATIVE
DISORDERS OF THE PERINEPHRIC SPACE
Cystic lesions
- Exophytic renal cyst or cystic lesions—including cystic neoplasms
and abscesses. - Urinoma—due to pelvicalyceal rupture, usually associated with
ureteral obstruction (e.g. stones), PUJO or trauma/surgery. - Lymphangiomatosis—rare benign lymphatic malformation
resulting in bilateral multiloculated perinephric cysts and usually
multiple bilateral peripelvic cysts
NEPHROGRAPHIC PATTERNS
Absent nephrogram
- 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. - Segmental—due to focal renal infarction (usually embolic
or vasculitic), focal pyelonephritis or an infiltrative lesion.
A rim of capsular enhancement, if present, indicates
infarction
NEPHROGRAPHIC PATTERNS
Unilateral delayed nephrogram
- Obstructive uropathy—e.g. ureteric stone/tumour.
- Reduced arterial inflow—e.g. renal artery stenosis, Page kidney
(reduced perfusion due to extrinsic compression by a subcapsular
haematoma or collection). - Reduced venous outflow—e.g. renal vein thrombosis or
compression. - Pyelonephritis—although a striated nephrogram is more
common. As opposed to the other differentials, pyelonephritis
does not result in a progressively hyperdense nephrogram.
NEPHROGRAPHIC PATTERNS
Bilateral persistent nephrogram
Both kidneys are still in the corticomedullary phase >90 seconds
or nephrographic phase >3 minutes after contrast injection.
- Reduced arterial inflow—e.g. systemic hypotension/shock, and
rarely bilateral renal artery stenosis. - 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. - Bilateral obstructive uropathy—rare.
- Reduced venous outflow—e.g. bilateral renal vein thrombosis.
Rare
NEPHROGRAPHIC PATTERNS
Unilateral striated nephrogram
Streaky radial bands of alternating hyper and hypoattenuation,
best seen in the excretory phase
- Acute ureteric obstruction.
- Acute pyelonephritis—may be unilateral or bilateral.
- Renal vein thrombosis.
- Traumatic renal contusion
NEPHROGRAPHIC PATTERNS
Bilateral striated nephrogram
- Acute pyelonephritis—may be asymmetrical.
- Abnormal renal tubules—e.g. acute tubular necrosis, acute
interstitial nephritis, tubular protein deposition (rhabdomyolysis,
HIV nephropathy). - Hypotension/shock*.Adrenals, urinary tract, testes and prostate 263
9 - 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. - Autosomal recessive polycystic kidney disease*—contrast
medium in dilated tubules
