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10.3 Pathology of the Kidney
347
ab
Fig. 10.23 Xanthogranulomatous pyelonephritis. Xanthogranulomatous pyelonephritis in a
child with distal renal acidosis and stone disease, longitudinal ( a ) and axial ( b ) section: complex-
cystic destruction of medullae, central calcifi cations, tumourously enlarged kidney, shape somewhat preserved
10.3.2.5 Tuberculosis
US / CDS Findings
Necrosis/atypical abscess – echogenic content, potentially with partial rim-like calcifi cations, commonly similar as complicated cyst. No other specifi c US/aCDS
fi ndings.
10.3.2.6 Xanthogranulomatous Pyelonephritis
Defi nition
Chronic infection, often with obstructive concretion/stone (“staghorn” shaped) that
leads to destruction of medulla, eventually of entire kidney.
US / CDS Findings
Regionally or diffusely thinned parenchyma and vasculature (aCDS), peripheral hyperaemia in membrane around abscess formation. Pseudotumourous aspect of destroyed
affected part. Disruption of normal renal parenchymal and vascular architecture in
abscess and necrosis; potentially perifocal hyperaemia around kidney (Fig. 10.23 ).
10.3.2.7 Glomerulonephritis/Nephrotic Syndrome
Defi nition
Large range of conditions.
US Findings
Commonly increased renal size, small medulla, enlarged cortex and potentially
increased echogenicity/reduced cortico-medullary differentiation, depending on
which compartments involved (Fig. 10.24 ).
Typically bilateral fi ndings:
• In chronic stage, kidneys may be small.
• In mild/atypical disease, kidney may look normal.
• Differentiation between various entities sonographically impossible.
• Other systemic fi ndings: ascites, pleural effusion – depend on degree of renal
failure/associated condition.
348
10 Ultrasound of the Urogenital Tract
ab
Fig. 10.24 Glomerulonephritis. ( a ) Swollen large right kidney (+ +) with small hypoechoic
medullae in acute but mild (postinfectious) GN (fi ndings bilateral, renal function normal). ( b )
A less-enlarged but still slightly swollen kidney with hyperechoic parenchyma and reduced
cortico-medullary differentiation in chronic recurrent GN (HUS may appear similar)
Consider renal manifestation of systemic disease such as lupus, HenochSchonlein purpura, amyloidosis, familiar Mediterranean fever, etc.
CDS Findings
Diffuse perfusion alterations – correlate more with degree of renal failure than with
underlying entity (except for primarily vascular conditions – see below).
Role of US
Initial diagnosis: exclude other conditions by validating pre-/postrenal causes of
renal failure. Assessment of renal perfusion, also during course of disease, as well as
secondary/associated changes (e.g. under haemofi ltration – intravascular
volume?).
US-guided biopsy for histological evaluation (see Fig. 2.13 ).
10.3.3 Vascular Conditions
Role of US in Renal Vascular Conditions
Most developed tool for screening, initial diagnosis and and follow-up. US most
useful for follow-up, differentiation against other renal conditions and monitoring
of future renal growth.
Will allow depiction of changes in perfusion patterns:
• However, if US potentially limited, then additional imaging necessary (see above).
• Algorithms recommended for certain conditions, e.g. imaging in suspected
childhood renovascular hypertension (see Pediatr Radiol (2010) 40:1315).
10.3.3.1 Renal Artery Stenosis
Defi nition
Rare in childhood, commonly not arteriosclerotic in origin but associated with other
vasculopathies, after vasculitis, trauma/surgery, by compression.
US Findings
• Using meticulous scanning techniques, entire course of extrarenal artery is often
visualised.
10.3 Pathology of the Kidney
Fig. 10.25 Renal artery stenosis. Elevated fl ow velocity with turbulent atypical fl ow at site of left
renal artery stenosis, also seen as aliasing of CDS signals and narrow vessel diameter
349
• Rarely changes in diameter or aneurysmal dilatation seen on gray scale.
• Intrarenal portions only assessable using CDS.
CDS
• Most striking fi nding: aliasing of colour spectrum – provided adequate scale settings.
• Always perform spectral analysis:
– At stenosis: marked increase in systolic velocity with spectral broaden-
ing + turbulent fl ow.
– Distal to stenosis: decreased systolic velocity, more or less normal to elevated
diastolic velocity, depending on severity/grade. Delayed systolic upstroke
with increased acceleration index (pulsus tardus et parvus) (Fig.
10.25 ).
– In kidney: sometimes aCDS depicts segmental hypoperfusion due to infarc-
tion of affected area after severe stenosis.
NOTE : Always assess all renal sectors (as in children intrarenal stenosis quite com-
mon) – peripheral and main segmental branches need to be seen on CDS for reliable
assessment. Always assess abdominal aorta/other low-resistive fl ow vessels (e.g.
coeliac trunk, cerebral vessels) to differentiate focal from systemic conditions.
Remember, that particularly in gray scale dissection may be hard to see; US does
not always allow exclusion of stenosis. In some conditions ce-US can enhance US
potential.
Additional Imaging
Captopril scintigraphy.
CT/MR angiography and catheter angiography with PTA/stenting.
350
abc
Fig. 10.26 Renal infarction. ( a ) Echogenic, more or less triangular-shaped segmental parenchymal
lesion in a child with sickle-cell anaemia, consistent with an infarction. ( b ) No vessels depictable by
aCDS in this traumatic renal infarction of parts of the kidney (dissection of supplying accessory artery).
( c ) Polar infarction (+ +) demonstrated by aCDS after sacrifi cing a polar artery during transplantation
10 Ultrasound of the Urogenital Tract
10.3.3.2 Arteriovenous Fistula (AVF)
Defi nition
Rarely spontaneous or idiopathic (vasculopathies), common after surgery, trauma,
biopsy.
US Findings
Large fi stula may show as cystic interruption of normal renal parenchymal structure.
Secondary sedimentation in renal pelvis due to haemorrhage.
Cortical infarct of dependent area.
CDS :
Most useful tool for depicting AVF.
• Adapt scale to become sensitive for aliasing (demonstrates site of AVF).
• Feeding artery hyperaemic with increased velocities/low RI; draining vein may
have increased velocities with arterialised fl ow spectrum– spectral analysis man-
datory (see Fig. 10.32 ).
• At AVF: unidirectional high-velocity turbulent fl ow.
• aCDS visualises focal peripheral perfusion impairment of dependent areas – risk
of infarction.
Additional Imaging
ce-CT/MRA. Catheter angiography – potentially with embolisation.
10.3.3.3 Infarction
Defi nition
Rare in childhood – posttraumatic, postoperative, postinterventional, in coagulopathies, other systemic disease such as haemolytic anaemia (e.g. sickle-cell anaemia).
US Findings
Initially diffi cult to differentiate from focal pyelonephritis but soon develops
increasingly sharp borders with triangular shape and rather echogenic parenchyma
(Fig. 10.26 ).
Eventually (necrosis) less echogenic, develop into scars – cannot be differentiated from other scars.
aCDS
Segmental perfusion defect; detection can be enhanced by intravenous ce-US.
10.3 Pathology of the Kidney
abc
Fig. 10.27 Renal vein thrombosis – typical US and CDS fi ndings. ( a ) Echogenic swollen kidney
in neonate with haematuria. ( b ) CDS with spectral trace exhibits high-resistance arterial fl ow; no
venous fl ow depictable. ( c ) Renal vein thrombus reaches into IVC
351
Additional Imaging
Only if of therapeutic consequence: ce-CT/MRI. Potentially scintigraphy.
10.3.3.4 Renal Vein Thrombosis
Defi nition
Rare, but exists even in neonates:
• Causes: posttraumatic, postoperatively, postinterventional, coagulopathies,
dehydration, systemic infection, tumourous/by local compression/displacement
(e.g. after neonatal adrenal gland haemorrhage with displacement of kidney – in
this condition always assess renal perfusion!).
• May often start peripherally, eventually grows into central veins – in early stages
central renal vein may be patent.
• Tumour thrombus (particularly Wilms tumour) may grow through renal vein into
IVC, up to right atrium. Risk of pulmonary embolism.
US Findings
• In central vein or IVC, thrombus formation is visualised replacing normal
anechoic lumen of then often distended vessel.
• Most striking – secondary changes in kidney: swollen, echogenic (regionally
pronounced = haemorrhage) and with disrupted cortico-medullary differentia-
tion (Fig. 10.28 ).
• Intrarenal thrombus cannot be visualised directly.
CDS
• Striking hypovascularisation of affected area/kidney; non-affected parts/central
vessel may still exhibit antegrade fl ow (often with bidirectional colour fl ow sig-
nals) (Fig. 10.27 ).
• Spectral trace in affected area – bidirectional arterial fl ow with short high-peak
systolic infl ow and diastolic backfl ow, which drains all systolic blood fl ow (no
effective antegrade perfusion).
• No venous colour signals/fl ow spectra depicted in affected area/vein(s).
352
abc
Fig. 10.28 Nephrocalcinosis. ( a ) Echogenic depositions in distal tubules close to papillae in a
neonate after furosemide therapy. ( b ) Echogenic outer layer of medulla in early (stage I) medullary
nephrocalcinosis. ( c ) Entire medullae calcifi ed, with shadowing – late stage of medullary neph-
rocalcinosis (stage III), but cortex is preserved (no global calcinosis) – kidney borders diffi cult to
depict, outlined (+ +
1, 2
)
10 Ultrasound of the Urogenital Tract
Role of US
In combination with clinical symptoms and signs, the typical US and CDS fi ndings
are diagnostic; no additional imaging needed or will reveal additional information.
Even in tumour thrombus, CDS is the most sensitive method; otherwise for assessment of thrombus of IVC, contrast-enhanced sectional imaging may be used.
10.3.4 Nephrocalcinosis
Defi nition
Precipitation of echiogenic, calcium containing material at cortico-medullary junc-
tion, tubules/papillae, cortex ....
Various causes: hypercalciuria, distal renal acidosis, Bartter syndrome, oxalosis,
secondary to other diseases (e.g. sickle-cell anaemia/sickle-cell nephropathy).
US = major imaging tool.
US Findings
Sonographically medullary nephrocalcinosis exhibits three stages (Fig. 10.28 ):
• Stage I: initially echogenic cortico-medullary transition zone.
• Stage II: increasing peripheral medullar echogenicity, increasing echogenicity of
papilla – eventually entire medulla echogenic. DDx of latter: remnant of papil-
lary necrosis.
• Stage III: entire medulla calcifi ed; fi nally also cortical deposits – increasing
echogenicity of entire kidney.
NOTE : Commonly nephrocalcinosis starts at medulla, not to be confused with
physiologic transient medullary / papillary echogenicity of neonates (transient,
resolves spontaneously).
Cortical forms initially cause increasing echogenicity of cortex (e.g. overdose of
Vitamin D).
Global nephrocalcinosis of cortex + medulla extremely rare in childhood, often
late stage of systemic disease, with additional urolithiasis/papillary necrosis, etc.
CDS
Twinkling sign – particularly in more advanced forms.
10.3 Pathology of the Kidney
353
Fig. 10.29 Urolithiasis. ( a ) Stone with shadowing in proximal ureter/pelvi-ureteric junction.
Kidney enlarged (+....+) and hyperechoic in acute obstruction by urolithiasis; some dilatation due
to recurrent episodes larger than usually seen in single acute event. ( b ) Same patient as in ( a ): subtle
twinkling of stone – not all stones exhibit vivid twinkling. ( c ) Stone (
mid-ureter – note change of calibre of ureter due to obstruction; ureter visible by using graded
compression following psoas muscle. ( d ) The twinkling sign depicts stone in proximal ureter, hard
to see on gray scale US (little shadowing and only slight distension of collecting system). Kidney
swollen, hyperechoic, with vague cortico-medullary differentiation in peri-acute stage
a
c
b
d
+ …+) with shadowing in
1
Role of US
• Mainstay of imaging.
• Depicts fi ndings in early stage (still negative on plain fi lm).
• Also used for follow-up.
• CT will also show deposit but not used due to radiation burden.
DDx
Similar gray scale fi ndings in atypical manifestation of congenital nephrotic syndrome
of Finnish type, ARPKD, renal vein thrombosis, cystinosis, oxalosis, glycogenosis and
tyrosinemia – these conditions must particularly be considered with atypical manifestation, visualising of other signs (e.g. tubular ectasia) and very early manifestation. Can
eventually also lead to calcifi cation of papillae (papillary calcinosis) and urolithiasis.
10.3.5 Urolithiasis
Defi nition
Less frequent in children than in adults – varying geographic distribution.
Number of underlying metabolic conditions to be considered.
Details of US appearance/value of additional imaging described above
(Sect. 10.3.2 ) (Fig. 10.29 ).
354
10 Ultrasound of the Urogenital Tract
NOTE : With increase in nephrocalcinosis, visualisation of urolithiasis within col-
lecting system and differentiation of urolithiasis versus papillary calcinosis will
become diffi cult.
10.3.6 Other Important Renal Parenchymal Disease
10.3.6.1 Haemolytic Uremic Syndrome (HUS)
Defi nition
Complication of bacterial enterocolitis; haemolysis congests renal vessels – causes
renal failure.
US Findings
Initially bilateral enlarged hyperechoic kidneys with small anechoic medullae.
Three stages differentiated:
• I: increased cortical echogenicity in relation to adjacent liver.
• II: even more increased echogenicity – still small hypoechoic medullae visible.
• III: completely hyperechoic kidney without cortico-medullary differentiation;
always associated with complete renal failure.
Further development depends on course of disease – from stepwise normalisation to cirrhotic kidneys with chronic renal failure (CRF).
CDS
• Nonspecifi c but helps to fi nd vessels for spectral analysis.
• Signs of increased resistance with low/inverted diastole, high systolic fl ow and
increased RI.
• Reduced venous fl ow.
NOTE : Doppler nonspecifi c. Always assess other vessels for comparison (renal
versus systemic/cardiac condition).
TIP :
Spectral analysis may help predict prognosis – perfusion patterns normalise prior to
normalisation of creatinine on blood samples, helpful in planning ongoing dialysis.
Additional Investigation
• Always assess entire abdomen – confi rm diagnosis of enterocolitis.
• Search for ascites/other complications.
• Eventually – in unclear cases/prognostic reasons – US-guided renal biopsy (pro-
vided normal coagulation).
• No other imaging performed.
10.3.6.2 Glomerulonephritis/Nephrotic Syndrome
See Sect. 10.3.2.7 above.
10.3.6.3 Scars, Cirrhotic Kidney
Remnants or residual of previous disease.
Cirrhotic kidney always associated with severe loss of renal function. If other
kidney healthy – contralateral hypertrophy (volume calculations essential).
Focal scars: usually after trauma or infection and infarction, defi ned by parenchymal
narrowing, caliceal clubbing, altered echogenicity and cortico-medullary differentiation – also see above (Sect. 10.3.2 ). Focal hypertrophy – hypertrophic Bertin columns.
10.3 Pathology of the Kidney
355
US / CDS Findings
• Diffusely/focal-altered echogenicity, variably clubbed caliceal system.
• Commonly increased echogenicity with reduced cortico-medullary
differentiation.
• Focal or diffuse reduced vasculature – however, RI may be normal.
Additional Investigations
• DMSA scintigraphy for split renal function (results with function <30 % less
accurate).
• IVU outdated.
• If aetiology unclear, consider VCUG/ce-VUS (if of therapeutic consequence).
• Increasingly MRI used for assessment of kidney/calculating split renal function.
10.3.7 Renal Failure (RF)
Defi nition
Acute or chronic, persisting or transient.
• Prerenal: systemic condition that impacts renal perfusion/function.
• Intrarenal: disease affecting renal parenchyma, also involvement of renal paren-
chyma in systemic disease (e.g. lupus).
• Postrenal: commonly severe obstructive uropathy.
US Findings
• Acute pre-/intrarenal failure exhibits large, swollen, echogenic kidneys + altered
cortico-medullary differentiation.
• Findings depend on age, severity and underlying disease.
• In polyuric phase, collecting system may be distended.
• In anuria collecting system collapsed.
• In chronic obstructive uropathy: dilated system.
• Chronic renal failure (CRF) depends on underlying disease – no specifi c fi ndings.
CDS
Particularly in early acute phases (asymmetrically?) elevated RI with low diastolic fl ow.
In chronic failure RI pseudonormal, with low fl ow velocities.
Role of US
Method of choice for initial diagnosis, follow-up and differentiating different kinds
of renal failure.
10.3.8 Renal/Urinary Tract Trauma
Grades (Table 10.4 ) with respective US Findings :
• Perirenal / subcapsular haematoma : intermediate homogeneous echogenicity,
may be diffi cult to differentiate from cortex. With duration increasingly
hypoechoic with sedimentation/clot formation, situated either subcapsular
(maintains shape of kidney) or perirenal. aCDS particularly valuable for early
stages, where gray scale may miss even signifi cant haematoma.
• Contusion : regionally altered parenchymal structure with increased echogenicity,
sometimes only seen after several hours. Even in early phases focally altered
vascular architecture on aCDS. Well seen on ce-US.
356
Table 10.4 Renal injury grading system (American Association for the Surgery of Trauma) –
according to depth of damage and involvement of urinary collecting system and renal vessels
Grade I Contusion or non-enlarging subcapsular haematoma, no
laceration
Grade II Superfi cial laceration <1 cm depth
Does not involve collecting system
Non-expanding perirenal haematoma
Grade III Laceration >1 cm
Without extension into renal pelvis or collecting system
With no evidence of urine extravasation
Grade IV Laceration extends to renal pelvis or urinary extravasation
Grade V Shattered kidney; devascularisation of kidney due to hilar
injury
10 Ultrasound of the Urogenital Tract
• Laceration : initially sometimes diffi cult to depict due to same phenomena as
above; may be improved by aCDS/ce-US. Always associated with perirenal haematoma, disruption of capsule, varying amount of retroperitoneal haemorrhage
and haemoperitoneum. Always try to assess whether major central structures are
affected (vessels, collecting system) – aCDS essential.
• Traumatic haematuria : only indirect signs (echoes within collecting system,
clots, disruption/thickening of pelvic wall) – US less sensitive, maybe ce-CT/MR necessary.
NOTE : In children, haematuria not predictive for kind, severity or prognosis of
renal injury!
• Hilar dissection : kidney looks sonographically normal. Only CDS reveals lack
of perfusion of kidney and disruption/alteration of fl ow at dissected/disrupted
vessel. Transection or disruption of ureter diffi cult to visualise – only depicted by
indirect signs such as urinoma formation.
• Posttraumatic changes : haematoma often resolve spontaneously, urinoma may
need drainage of collecting system (do not drain urinoma itself!). Secondary
scars, complex cysts, calcifi cations, posttraumatic aneurysm/AVF, shrinking
kidneys, etc.
Role of US
• First investigation in emergency room ( FAST ).
• Detailed US study in mild/moderate urinary tract trauma (always include CDS)
10.30 ).
(Fig.
• Method of choice for follow-up in most of conservatively treated patients (see
ESUR/ESPR recommendations for imaging childhood renal trauma – Pediatr
Radiol (2011) 41:939).
Additional Investigations
• In acute severe (poly)trauma = ce-CT.
• For follow-up, in complex/subacute situations = MRI.
• Rarely catheter angiography (potential recanalisation of renal vessels in central
vessel compromise).
• Follow-up by US, DMSA scintigraphy, MRI.