You are on page 1of 5


Acute pyelonephritis. This is an acute bacterial infection of the upper urinary tract. It is largely due to
ascending infection with gram-negative bacili (most commonly Escherichia colli) and is associated
with cystitis. It commonly affects females throughtout adult life (when the urinary tract is otherwise
usually normal) but is relatively uncommon in young adult males unless there is a structural or
functional lesion of the urinary tract, such as inadequate bladder emptying. In order males it becomes
more frequent in association with benign prostatic disease and consequent bladder outflow
obstruction. It presents with pyrexia, loin pain and tenderness and often symptoms of cystitis.
Acute pyelonephritis requires no immediate investigations and is usually resolving within 72 h on
appropriate antibiotic treatment. If the clinical picture is not improving by this stage, further imaging
is required to investigate the possibility of an abcess (ultrasound or CT) or obstruction (ultrasound
and/or IVU). Usually the IVU is normal. In one-third of cases, however, where the inflammatory
process and oedema are more severe, IVU may show some of the following features. The kidney may
be smoothly enlarged and the calyces compressed by the adjacent swollen parenchyma. The affected
kidney may show reduction in perfusion and function and a striated nephrogram. Rarely in infecting
bacteria release an endotoxin that relaxes the smooth muscle of the ureter, which stops peristalsis, and
the ureter dilates. This may cause considerable concern, as if obstruction is suspected in the context of
infection, relatively prompt drainage of the collecting system is required, usually by nephrostomy.
Differentiation of obstructive from non-obstructive dilatation can be difficult but if there is genuine
obstruction with infection there is usually significant delay in excretion of contrast on the IVU, or
even on excretion from the affected kidney over several hours. On the other hand, if contrast appears
within the collecting system within 5 or 10 min it is highly unlikely to be significantly obstructed.
Similarly, ultrasound and MRI will often be normal but with more severe cases will show smooth
renal enlargement. Ultrasound may show some diffuse reduction in enchogenicity. Contrast-
enchanced CT may demonstrate perinephric oedematous or inflammatory change. In a significant
number of cases the pyelonephritic process is focal rather than diffuse and leads to an area of lacalised
swelling and reduced function within the parenchyma, which may appear as a mass of medium to low
echogenicity on ultrasound (Fig.30.33) and medium to low density on CT. When severe, this may
appear as a mass on IVU, compressing the adjacent calyces. The older term for this lesion is acute
lobar nephronia but it is more logical to refer to it as focal ppyelonephritis. These features return to
normal after the acute episode. An area of severe localised pyelonephritism however, may progress to
abcess formation. Following an acute episode of pyelonephritis the patient should be investigasted to
look for an underlying cause, particularly calculi, PUJ obstruction, inadequate bladder emptying and
Emphysematous pyelonephritis. This uncommon condition is a severe pyelonephritis with a gas-
producing organism (generally Gram-negative bacilli, especially E.coli), usually in elderly diabetic
patients and frequently associated with ureteric obstruction. Gas develops within the renal
parenchyma and may also spread to be perinephric space. There is often enough gas present to enable
the diagnosis to be made on the plain film. CT, however, is more sensitive and will more accurately
demostrate the distribution of the gas. If it is diffusely throughout the kidney then
emergencynephrectomy is indicated. Renal function will already have been destroyed and without
surgery mortality may be in excess of 50%. If gas is localised to one part of the renal parenchyma a
conservative approach with intravenous antibiotics and consideration of CT-guided drainage may be
appropriate. Gas in the pelvicalyceal system and ureter without gas in the renal parenchyma represents
emphysematous pyelitis and can also be managed conservatively (Fig.30.34). It is worth mentioning
for completeness that gas bubbles may be encountered in the collecting system in the absence of
infection if they have gained access at the time of surgical instrumentation of the urinary tract
(catheterisation, retrograde pyelography, etc.), or in the presence of a fistula to the skin or a gas-
containing viscus (Fig. 30.35).
Renal abscess. Focal renal parenchymal inflammation may progress to liquefaction and abscess
formation. This may be the sequel to untreated or resistant acute pyelonephritis or haematogenous
spread of infection. The former is usually due to Gram-negative or anaerobic bacili, the latter to
Staphylococcus aureus and associated with a septic site elsewhere (skin or nasal cavity focus,
intravenous drug abuse, infected central line) or impaired immunity, including diabetes.
Haematogenous spread may lead to multiple and/or bilateral renal abscesses as well abscesses else-
where in the body (particularly consider vertebral, pulmonary and cerebral metastatic spread). There
may be marked loin pain and tenderness and severe pyrexia. IVU usually shows only a non-specific
mass. The condition is better imaged with ultrasound or CT, which will show a heterogeneous mass
(with irregular marginal enchancement on CT) containing single or multiple central areas of cyctic
necrosis (Fig. 30.36). There is often considerable echogenic debris within the cystic areas on
ultrasound. In severe cases gas may appear, best seen on CT. Perinephric inflammatory disease may
also be identified.
Where there is a substantial liquefied area, ultrasound or CT-guide positioning of a percutaneous drain
may be useful. However, these patients often come to imaging at a relatively early stage of
development of the abscess with only a tiny area of liquefaction demonstrable (2 cm or less). It is
likely that these patients are better served by intravenous antibiotics and subsequent scanning to
monitor resolution rather than premature intervention.
Perinephric abscess. Renal infection of any severity may be associated with extension of disease into
the perinephric space with the formation of a perinephric abscess. On IVU there is only indirect
evidence such as loss of the psoas shadow, poorly seen renal outline and reduced or absent renal
function manifested by failure to excrete or concentrate contrast. Ultrasound and CT will demonstrate
a fluid or semifluid collection, often containing debris and septations and sometimes gas in the
presence of the appropriate organism (Fig. 30.37). Further extention of infection is largely determined
by the anatomy of the retroperitoneal fascial planes. Although disease may extend in any direction
(including medially across the midline into the contralateral perinephric space), the course most often
taken is directly posteriorly through the posterior perinephric fascia into the posterior perirenal space.
From this site, further extension is often laterally into the lateral extraperitoneal space and lateral
abdominal wall, posteriorly through the transversalis fascia into the psoas and quadratus lumborum
muscle and inferiorly along the psoas and then iliacus muscles into the pelvis.
Pyonephrosis. Infection of an obstructed kidney may lead to pus developing within the renal pelvis
and calyces (pyonephrosis). It may occur in association with any cause of obstruction but most
frequently in the presence of calculi or the condition of undiagnosed PUJ obstruction. The imaging
features are those of an obstructed system with particularly, early or severe loss of renal function.
Cross-sectional iamging may show evidence of thick pus and/or inflmmatory debris within the dilated
pelvicalyceal system (for example, echogenic areas on ultrasound or increased density on CT with
posible layering). The infecting organisms are most commonly Gram-negative bacili from ascending
infection. Untreated, there is a danger of septiceamia, destruction of normal renal tissue and extension
into surrounding areas. Treatment is by percutaneous drainage. This should only be performed with
adequate antibiotic cover and a minimum of manipulation, as Gram-negative septicaemia and
endotoxic shock are recognised and life-threatening complications of the procedure. Sometimes the
situation develops insidiously over a considerable period of time, particulary in the elderly, and may
then be associated with cortical loss and perinephric disease (Fig. 30.38).
Xanthogranulomatous pyelonephritis. This is a chronic inflammatory process in which lipid-laden
histiocytes invade and replace normal renal parenchyma. It is seen in the context of chronic urinary
infection, usually with calculi, which initiates and propagates the disease. The infecting organism is
usually E. Coli or Proteus mirabilis. There is marked female preponderance and 10% of patients are
On IVU there is a non-functioning kidney, with calculi present in around 80%. Characteristically this
is laminated or branched and fragmented. Initially the kidney may be enlarged and this may have a
focal pattern simulating tumor (tumefactive xanthogranulomatous pyelonephritis) but ultimately there
is renal atrophy, which may be marked. Ultrasoud and CT show loss of normal corticomedullary
differentiation and heterogeneity, which includes debris-containing systic areas and calculi. The
disease usually extends into the perinephric space with obliteration of tissue planes on all madalities.
(Fig. 30.39). With further extension through the layers of perinephric fascia the disease may extend
into psoas muscle and the abdominal wall with the formation of a cutaneous fistula. Internal extension
potentially leads to enteric fistulas. Enchancing areas of parenchyma may survive around the cystic
areas, mimicking hydronephrosis. Where there is doubt a retrograde examination will show a
contracted pelvicalyceal system and the absence of high-grade obstruction.
Tuberculosis. Renal involvement is a feature of postprimary tuberculosis. Reactivation occurs at the
corticomedullary junction. There is local infiltration into the parenchyma with subsequent papillary
necrosis. Bacilli enter the collecting system and pyuria develops. Further progress of the disease is
characterised by multifocal stricturing with impairmant of drainage, formation of caseos pus and
subsquent calcification. The classical features are seen on IVU. Strictures affect the calyceal necks,
with the formation of hydrocalyces. Furhter strictures may be seen at the PUJ and at multiple levels in
the ureter. The pelvis itself may become contracted. Significantly obstructed calyces accumulate pus
and there is loss of parenchyma due to a combination of obstruction by the inflammatory process.
Damage areas and the caseous pus subsequently calcify. Badly affected areas become non-functioning
(Fig. 30.40). When the pelvis is affected the entire hydronephrotic kidney may become non-
functioning (tuberculous autonephrotomy). Ultrasound and CT will demostrate hydrocalyces and/or a
hydronephrosis, which may contain a considerable amount of debris, areas of calcification and
parenchymal loss. Bacili pass into the bladder, which also becomes inflamed and subsequently
contracted. Presentation is usually with frequency and urgency. Although tuberculous lesions with
subsequent calcification my develop at any site in the urinary tract, as a general rule the radiological
changes are more pronounced in the upper urinary tract (kidney and ureters), as againts those seen
with schistosomiasis, which predominates in the lower urinary tract.
Schistosomiasis. Urinary tract schistosomiasis is caused by a parasitic blood fluke. It predominately
affects the bladder but in up to 30% of cases also involves the ureter, particullarly distally. Ureters are
usually involved billaterally but often asymmetrically. Parasitic ova deposited in the ureteric wall
provoke an inflammatory reaction. In the early stage this may appear as multiple small inflammatory
polyps. In the established disease the appearences are of strictures, often multiple, and linear
calcification (Fig. 30.41).
Hydatid disease. This arises from parasitic infection with the dog tapeworm Echinococcus granulosus.
The usual intermediate hosts are pastoral animals, especially sheep. Tapeworm eggs from the dog
faeces are inadvertendly consumed and develop into larvae in the intestine of the intermediate host.
They pass through the intestinal wall and are disseminated the body. They particularly infect the liver,
rarely the kidney. The larvae develop into cysts. The wall of the cyst may calcify. On imaging, the
classical appearance is of a multioculated cystic mass, often with a dominant central cyst and multiple
daughter cyst. Occasionally communication with the collecting system is visible on contrast studies.
Reflux nephropathy. In this condition renal cortical scarring develops in association with dilated
calyces, It is due to severe vesicoureteric reflux (VUR) and urinary tract infection in childhood.
Because of its intimate relationship to VUR, it is worth considering this first.
Normally the ureter enters the superolateral angles of the trigone, penetrating the bladder wall at an
oblique angle, giving rise to an oval ureteric orifice. This acts as a valve, preventing urine refluxing
from the bladder into the ureter during micturition, the rise in intravesical pressure tending to close the
orifice. In a small proportion of children the ureter takes a more direct course through the bladder
wall, leading to a short intramural section and a round ureteric orifice which prediposes to reflux.
Usually this is an isolated defect (although some cases are familil) but it is also encountered in
association with a duplex system (usually the orthotopically inserted ureter of the lower moiety,
sometimes the ectopic upper pole poiety ureter) and some other structural developmental lesions
(prune-belly, parauteric diverticulum). Although there remains some controversy, it seems most
lakely that VUR leads to reflux nephropathy only when it is severe enough to be associated with
intrarenal reflux and ionfection. The insult to the kidney provokes scarring over the worst-affected
A grading system for VUR has been developed based on the appearences at micturating
cystourethrography (MCUG). It is given below for reference :
IReflux into the ureter alone; subdivided into reflux into part of the ureter only (Ia), all of the ureter
without dilatation (Ib) and with dilatation (Ic)
IIReflux into the ureter and pelvis; subdivided into complicate ureteric opafication without (IIa) and
with (IIb) focal dilatation and complete ureteric opafication (IIc)
IIIReflux into ureter and pelvis with mild dilatation; subdivided into fornices preserved (IIIa) and
midly blunted (IIIb)
IVReflux into ureter and pelvis with moderate dilatation and papilae; subdivided into partial (IVa)
or complete (IVb) forniceal obliteration
VReflux into ureter and pelvis with obliteration of the papillae; subdivided into subtotal papillary
obliteration (Va) and total papillary obliteration with severe (Vb) or extreme (Vc) pelviureteric
The more severe grades of reflux are demonstrable with radionuclide or ultrasound cystography.
Usually the child presents with urinary tract infection (or septicaemia if severe) and managament is
generally conservative, aiming to control urinary tract infection and avoid its recurrence.
Consequently intrusive investigation with MCUG (and the detailed grading described above) is
uncommonly required and surgery rarely indicated. VUR has a tendency to improve with age and new
scars not thought to develop after 5 years of age.
Reflux nephropathy is usually assymetrical or unilateral. The classical IVU appearances are of
cortical scarring over clubbed calyces. This is most frequently seen at the renal poles, especially the
upper pole because these are the sites of occurrence of compound calyces which are most susceptible
to damage from reflux. The relationship of the scarring to underlying abonormal calyces differentiates
the condition from vascular scarring and fetal lobulation (when the calyces are normal and, in the case
of lobulation, the indentations are between calyces rather than directly over them). Badly affected
kidneys grow poorly and are small, with diffuse cortical loss (Fig. 30.42). Severe continuing reflux in
childhood may show capacious significant reflux is rare. Presentation of reflux nephropathy in adults
is usually with recurrent urinary tract infection (which may be associated with pyelonephritis). If the
nephropathy is severe, patients may present with hypertension and/or renal insufficiency. Focal areas
of compensatory parenchymal hypertrophy may occur between the scars and, if prominent, may give
rise to concern about the presence of a tumour, although on ultrasound or CT their appearence is of
normal parenchyma. Ultrasound, CT and radionuclide imaging (DMSA) will all demonstrate the areas
of scarring.
Although reflux nephropathy does not develop in the adult kidney in the way it does in childhood, a
related condition is seen in patients with some lower urinary tract surgical procedures that permit
long-term significant refux of potencially infected urine. The ureters and pelvicalyceal systems dilate
and there is progressive diffuse loss of renal cortex and function. The condition is usually bilateral,
although it may show considerable asymmetry. It is most commonly seen with an ileal conduit (Fig.
30.34) but it also encountered in other procedures, especially those involving ureteric reimplantation,
for example uterosigmoidostomy.
Rare inflammatory conditions
Pyeloureteritis cystica is an uncommon condition associated with chronic obstruction and/or infection.
Multiple subephithelial cysts develop in the renal pelvis and/or ureter (usually the upper third)
generally 1-4 mm in diameter (occasionally up to 20 mm) (Fig. 30.44). They appear as well-defined
filling defects on IVU and retrograde pyelography. They are completely benign and asymptomatic,
the patient presenting with symptoms from the associated condition. They may persist for month or
years, even after removal of the cause.
Leucoplakia and malacoplakia are rare conditions seen in association with chronic urinary tract
infection. They can affect any part of the urothelium but are more commonly seen in the bladder.