Kidneys
RENAL PARENCHYMAL DISEASE
it is usually primarily renal but may be part of a systemic vasculitis (e.g. SLE, PAN, Goodpasture’s or Wegener’s)
no papillary or calyceal abnormality
smooth, normal pelvicalyceal systems 
prominent renal sinus fat
it usually follows an episode of severe ischaemia associated with hypotension, dehydration, or nephrotoxin exposure
increased echogenicity within the cortex and pyramids
little or no filling of the pelvicalyceal system
the insult is more severe than that seen with ATN and is usually due to obstetric shock
chronic: cortical calcificationPAPILLARY NECROSIS
diabetes 
sickle-cell disease or trait 
obstruction complicated by infection 
acute infection 
haemophilia 
renal vein thrombosis 
acute renal failure in infancyCT/IVU
• There is usually bilateral symmetrical involvement – unilateral involvement can occur with ascending infection or renal vein thrombosis 
the papillary and calyceal changes are rarely uniform
Acute: enlarged affected kidneys
Chronic: renal atrophy with a regular type of surface scarring (due to atrophy of the cortex overlying the damaged papillae and hypertrophy of the intervening columns of Bertin)
‘Lobster claw deformity’: initially the necrotic areas erode the papilla tip and excavate from the fornices into the pyramids
‘Egg in cup’ appearance: with progression contrast curves around the papilla from both fornices
• Papillae: the papilla initially swells and may eventually slough into the pelvicalyceal system causing colic, haematuria or hydronephrosis (as it appears as a filling defect it can mimic tumour, calculus or a blood clot) 
if the papillae fail to separate (necrosis in situ) the calyces may appear normal 
the papillae may calcify (with spotty calcification in a ring or triangle around a translucent centre)
• Remaining defect: calyceal clubbing resulting from a flattened or concave pyramidal tip
it is usually bilateral (but can be unilateral or segmental)
phaeochromocytoma 
horseshoe kidney 
Caroli’s disease 
hemihypertrophy
cortical scarring (representing parenchymal loss) with underlying clubbed calyces 
localized scars are more common within the upper pole (R>L)NEPHROCALCINOSIS
CT/IVU
• Medullary nephrocalcinosis: this is usually the product of a metabolic disorder resulting in a raised serum calcium or a tubular defect resulting in hypercalciuria 
calcification is usually bilateral and diffuse
• Cortical nephrocalcinosis: this is seen in acute cortical necrosis of any cause 
calcification is usually punctate and patchy (classically with a ‘tramline’ appearance)
Glomerulonephritis  acute tubular necrosis  acute cortical necrosis |
No papillary or calyceal abnormality  no focal cortical loss |
Papillary necrosis  medullary sponge kidney  megacalycosis/polycalycosis |
Papillary or calyceal abnormality  no focal cortical loss |
Obstructive nephropathy  focal reflux nephropathy |
Papillary or calyceal abnormality  focal cortical loss |
| Site | Cause |
| Cortical | Acute cortical necrosis |
| Medullary | Associated with a metabolic disorderHyperparathyroidismSarcoidosisDrug related (e.g. hypervitaminosis D, milk-alkali syndrome)MyelomatosisPrimary or secondary hyperoxaluriaHyperhyroidismOsteoporosis |
| Associated with renal tubular defectsIdiopathic hypercalciuriaMedullary sponge kidneyRenal tubular acidosis | |
| Focal | Linear or rim calcificationRenal artery aneurysmReal cyst |
| Amorphous calcificationCalcified haematomaTuberculosisRenal cell carcinoma (in 10%)Calcified renal papilla |
RENAL TRACT INFECTION/INFLAMMATION
ACUTE PYELONEPHRITIS
DEFINITION
• Bacteriuria, pyrexia and flank pain due to an ascending infection in 85% (usually E. coli), or haematogenous seeding in 15% (S. aureus)
vesicoureteric reflux (VUR) 
urinary obstruction 
pregnancy 
instrumentation 
immune deficiency
it can however be useful if the diagnosis is in doubt or to exclude obstruction or abscess development
delayed and poor pelvicalyceal system filling 
a dense, persistent or striated nephrogram (with severe disease)
the affected segments are hypoechoic (they can be hyperechoic with haemorrhage) 
reduced corticomedullary differentiation (due to oedema) 
focal or diffuse reduced perfusion
renal swelling with acute disease
any abnormal parenchymal enhancement may persist for > 2 months and may develop into a scar
emphysematous pyelonephritis 
xanthogranulomatous pyelonephritis 
cortical atrophy and renal failure
fungal infections 
glomerulonephritis 
interstitial nephritisRENAL TUBERCULOSIS (TB)
DEFINITION
• The kidneys are the 2nd commonest site of TB involvement after the lung (even though the CXR is normal in 35–50% of cases it usually follows haematogenous spread from the lung)
papillary ulceration occurs early, with later spread to the collecting system leading to fibrosis and stricture formation
haematuria 
sterile pyuriaRADIOLOGICAL FEATURES
IVU/CT
Although both kidneys are seeded, clinical manifestations are usually unilateral (> 70% of cases)
• Early: an enlarged kidney 
irregularity and destruction of ≥ 1 papillae (resembling papillary necrosis)
Renal calcification (30%): this appears as punctate or curvilinear renal parenchymal calcification or as calcification within a caseous pyonephrosis (with a characteristic cloudy appearance in the distribution of the dilated calyces)
– ‘Tuberculous autonephrectomy’: this may progress to homogeneous calcification within a dilated pelvicalyceal system so that the kidney appears as a lobulated calcified mass
Ureteric calcification: this is the 2nd commonest site of calcification with a typical beaded appearance 
calcification of the bladder, vas deferens and seminal vesicles is rarely seen
Cavitations: these are usually irregular and communicate with the collecting system 
widespread cavitations may mimic hydronephrosis (but the pelvis and infundibula of the calyces are not dilated unless there is an associated obstruction)
Fibrotic strictures: these can occur anywhere within the renal tract
– Hydrocalycosis: a local calyceal dilatation due to a partial stricture of a major infundibulum (the infundibulum appears ‘cut off’ with a complete stricture)
– Ureter: a ‘corkscrew’ appearance (due to multiple stenoses) 
a ‘pipestem’ appearance (due to a rigid and aperistaltic ureter)
– Early: trabeculation 
bladder wall irregularity 
a slight decrease in capacity
– Late: a thick-walled small-capacity bladder demonstrating calcification 
bladder TB is almost always associated with renal TB 
often there is VUR into a widely dilated upper tract
it is associated with diabetes and obstruction
there is a high mortality rate (> 60%) and it may require nephrectomy
it has a lower mortality rate, and percutaneous drainage and antibiotics may be sufficient
the patient is usually diabetic
XANTHOGRANULOMATOUS PYELONEPHRITIS (XGP)
DEFINITION
• Chronic renal parenchymal inflammation with replacement of the normal renal parenchyma with lipid-laden histiocytes 
it is secondary to chronic urinary infection (e.g. E coli or Proteus mirabilis) and obstructing calculus disease 
it is associated with diabetes
the focal form can mimic a tumourRADIOLOGICAL FEATURES
IVU/US/CT
A renal staghorn calculi (70%) 
an enlarged (global or focal) non-excreting kidney 
dilated affected calyces with internal echoes or debris 
a heterogeneous kidney with multiple non- or rim-enhancing low attenuation areas (−15 to −20 HU) representing dilated calyces and xanthomas 
perinephric extension (± a thickened Gerota’s fascia)
RENAL ABSCESS
DEFINITION
• A renal parenchymal collection secondary to acute pyelonephritis (Gram-negative or anaerobic bacilli) or haematogenous spread of infection (S. aureus)
RADIOLOGICAL FEATURES
CT
There is a heterogeneous central portion of near-fluid density (with no enhancement) 
there are enhancing thick irregular walls (± perinephric inflammatory change) 
gas within the lesion is diagnostic
absent renal function
this may extend in any direction
SQUAMOUS METAPLASIA, LEUKOPLAKIA, MALACOPLAKIA, AND CHOLESTEATOMA
DEFINITION
it is associated with recurrent urinary tract infections and calculi
it appears as thickened folds and irregularity of the renal pelvis
small plaques are visible on the mucosal surfaces (bladder > upper urinary tract)
there may be impaired renal function if the parenchyma is involved
it is associated with urinary tract infection and chronic obstructionBILHARZIA (URINARY SCHISTOSOMIASIS)
DEFINITION
• This is due to a fluke infestation (Schistosoma haematobium) 
the worm enters the skin and matures within the liver (via the portal vein) 
ova are then deposited within the bladder or ureteric submucosa (via the perivesical plexus) 
the ova produce an inflammatory reaction, leading to granuloma and stricture formation
there can be multiple filling defects (representing granulomas or ureteritis cystica) 
parallel lines of ureteric calcification can be seen
diabetics are at increased risk
it is highly echogenic on US, and it may demonstrate air within the collecting system and bladderPYONEPHROSIS
DEFINITION
• Pus within the renal pelvis and calyces following an ascending infection in an obstructed kidney (e.g. secondary to a calculus or PUJ obstruction) 
there is a risk of septicaemia and endotoxic shock (especially with attempted drainage)
RADIOLOGICAL FEATURES
debris or gas (dense shadowing) within the renal pelvis 
cortical loss or a perinephric abscess if long-standingCT
High-density material (± layering) within a dilated pelvicalyceal system 
there may be a renal or perinephric abscess
RENAL ARTERY STENOSIS (RAS)
RENAL ARTERY STENOSIS (RAS)
DEFINITION
the resultant increased renin (and angiotensin II) levels leads to vasoconstriction
atheroma involves the origin (ostial) or proximal ⅓ of the renal artery 
there can be post-stenotic dilatation
renal arterial lesions are caused by eccentric atheromatous plaques of the proximal renal arteryFibromuscular dysplasia (FMD)
• This is the most common cause of a non-atheromatous RAS and is the 2nd most common cause of an RAS (15–20%) 
it typically occurs in young women
• Medial fibroplasia is the commonest form, causing multiple short stenoses (with a ‘string of beads’ appearance on angiography)
• It involves the distal main renal artery (and its major branches) 
it can also affect the external iliac and carotid arteries
aortic disease may consist of diffuse or focal stenoses, occlusion, or a fusiform AAARADIOLOGICAL FEATURES
a renal artery to aortic velocity ratio (RAR) > 3.5 
a ‘parvus and tardus’ effect within the intrarenal vessels (due to velocity reduction and slowing of the acceleration of the systolic upstroke)
it has a sensitivity (97%) and specificity (92%) comparable with intra-arterial angiography for detecting stenoses within the main and segmental arteriesDSA
Formally the gold standard 
it is increasingly being replaced by non-invasive methods
• An aortogram is essential to demonstrate the number and location of the renal arteries and also the presence of any aortic or proximal renal vascular abnormalities
• Selective arteriography should not be performed in RAS (except as a prelude to renal angioplasty) as it may cause renal artery dissection or occlusion
PEARLS
Renal angioplasty and stenting
• The kidney must be salvageable (e.g. a renal length > 8cm and a satisfactory GFR) 
the best results are obtained with FMD
• Indications: resistant hypertension 
renal failure 
flash pulmonary oedema
• Complications (with a greater potential than seen in peripheral vascular disease): renal artery rupture and perforation 
branch occlusion 
occlusion of the main renal artery 
cholesterol emboli 
a short-term deterioration in renal function (due to the contrast medium given)
Middle aortic syndrome
A rare condition whereby renal artery stenoses are associated with abdominal aortic coarctation (± visceral artery stenoses) 
it may be associated with Williams’ syndrome or neurofibromatosis
blue line, left kidney).*RENAL VASCULAR ABNORMALITIES
RENAL ARTERY ANEURYSMS
DEFINITION
mycotic 
post-traumatic 
atherosclerotic 
vasculitic 
fibromuscular hyperplasia
both will demonstrate aneurysmal dilatation
absent wall calcification 
occurring during pregnancy
aneurysms tend to be more peripheral than with FMDARTERIOVENOUS MALFORMATIONS AND FISTULAE
DEFINITION
• These are usually iatrogenic or post-traumatic (but can rarely be congenital) 
it may lead to impaired renal function due to a ‘steal’ effect
TREATMENT
RENAL VEIN THROMBOSIS
DEFINITION
• Renal vein occlusion by thrombus can be caused by: membranous glomerulonephritis (the commonest adult cause) 
nephrotic syndrome 
dehydration 
hypercoagulable states 
renal or left adrenal tumours
with chronicity venous collaterals can open with only slightly impaired renal functionRADIOLOGICAL FEATURES
IVU
• Acute: an enlarged kidney 
a faint or absent nephrogram 
absent pelvicalyceal filling (which may also be stretched and compressed by an oedematous renal parenchyma) 
rarely there may be an increasingly dense nephrogram (± striations)
• Chronic: a normal or atrophic kidney 
retroperitoneal venous collaterals can indent the PC system
renal vein thrombus and a lack of flow within the main veins (± reversed end diastolic flow within the parenchymal veins)
prolonged irregular parenchymal enhancement 
prolonged corticomedullary differentiation 
the ‘cortical rim’ sign 
delayed or absent contrast medium excretion
3D gadolinium-enhanced MRA may differentiate benign from tumour thrombus
selective renal venography may identify any filling defectsRENAL INFARCTION
DEFINITION
• Thromboembolic occlusion of a renal artery usually leads to a focal renal infarction (less commonly total infarction) 
over time the infarcted area decreases in size with scar formation and tissue retraction
aortic aneurysm 
trauma 
thrombosis (due to atheroma or vasculitis)RADIOLOGICAL FEATURES
this can progress to a shrunken end-stage kidney
there is failure of tracer uptake on later images
T1WI + Gad: no enhancementDSA
This defines the site of any arterial block
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