Acute pyelonephritis This is an acute bacterial infection of the upper urinary tract.

It is
largely due to ascending infection with Gram-negative bacilli (most commonly Escherichia
coli) and is associated with cystitis. It commonly affects females throughout 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 older males it becomes more frequent in association with benign
prostatic disease and consequent bladder outflow obstruction. It present with pyrexia, loin
pain, and tenderness and often symptom of cystitis.
Acute pyelonefritis requires no immediate investigation and is ussualy 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 ( US or CT) or
obstruction (US and/ or IVU). Ussualy the IVU is normal. In one-thirds of cases, however
where the inflammatory process and oedema are more severe, IVU may show some of the
following feature. The kidney maybe smoothly enlarged and the calyces compressed by the
adjacent swollen parenchyma. The affected kidney may show reduction in perfussion and
function and a striated nephrogram. Rarely the infecting bacteria release an endotoxin that
relaxe the smooth muscle of the ureter, which stops peri- as if obstruction is suspected in the
context of infection, relatively prompt drainage of the collecting system is required, ussualy
by nephrostomy. Differentiation of obstructive from non obstructive infection there is
significant delay in excretion of contrast. Infection the IVU, or even on excretion from the
affected kidney over several hours. On the other hand, if contrast appears within the
collecting system 5 or 10 min it is highly unlikely to be significantly obstructed. Similiarly
US and MRI will often be normal but with more severe cases will show smooth renal
enlargement. US may show some diffuse reduction in echogenicity. Contrast-enhanced CT
may demonstrated a striated nephrogram, global reduction in perfussion and function or
wedge shaped area of abnormality and is more sensitive than IVU in showing these changes.
CT may also demonstrate perinephric oedematous or inflamatory change. In a significant
number of causes the pyelonephritic process is focal rather than diffuse and leads to an area
of localised swelling and reduced function within the parenchyma, which may appear as a
mass of medium to low echogenity on US and medium to low density on CT. When severe,
this may appear as a mass on IVU, compressing the adjacent calyces. The older term of this
lession is acute lobar nephronia but it is more logical to refer to it as focal pyelonephritis.
These features return to normal after the acute episode. An area of severe localised
pyelonephritis, however, may progress to abcess formation. Following an acute episode of
pyelonephritis the patient should be investigated to look for an underlying cause, particularly
calculi, PUJ obstruction, inadequate bladder emptying and diabetes.

Emphysematous pyelonephritis. This uncommon condition is a severe pyelonephritis with a

gas producing organism (generally Gram negative bacilli, especially E. Coli(, ussualy in
elderly diabetic patient and frequently associated with ureteric obstruction. Gas develops
within the renal parenchyma and may also spread to the perinephric space. There is often
enaough gas present to enable the diagnosis to the made on the plain film. CT, however, is
more sensitive and will more accurately demonstrate the dostribution of the gas, if it is
diffusely throughout the kidney then emergency nephrectomy is indicated. Renal function
will already have been destroyed and without sugery mortality may be in excess of 50%. If
gas is localised to ne part of the reanl parenchyma a conservative approach with in antibiotic
and consederation of CT guided and the ureter dilates. This may cause considerable concern,
guided drainage mey be appropriate. Gas in the pelvicalyces system and ureter without gas in
the renal parenchma represents emphysematous pyelitis and can also be managed
conservatively. It is worth mentioning for completeness that gas bubbles can be difficult but if
there is genuine obstruction with bubbles may be encountered in the collecting system in the
absences of the urinary tract (cathetexation, retrograde pyelography, etc) or in the presence of
a fistula of the skin or a gas containing viscus.

Renal abcess. Focal renal aprenchymal inflammation may progress to liquefaction and
abcess formation. This may be the sequel to untreated or resistant acute pyelonephritis or
hematogenous spread infection. The former is ussualy due to Gram negative or anaerobic
bacilli, the latter to S. Aureus and associated with a septic site elsewhener (skin or nasal
cavity focus, iv drug abuse, infected central lne) or impaired immunity, including diabetes.
Haematogenous spread may lead to multiple and or bialteral reanal abcesses as well as abcess
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 nonspecific mass. The condition is better imaged with ultrasound or CT, which
will show a heterogeneous mass (with irregular marginal enhancement on CT) containing
single or multiple central areas of cystic 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 Ctguided positioning of a percutaneous drain may he
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 organisms (Fig. 30.37).
Further extension of infection is largely determined by the anatomy of the retroperitoneal
fascia) 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
Iumborum muscles 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 imaging may show evidence of thick pus and/or
inflammatory debris within the dilated pelvicalyceal system (for example, echogenic areas on
ultrasound or increased density on CT with possible layering). The infecting organisms
are most commonly Gram-negative bacilli from ascending infection. Untreated, there is a
danger of septicaemia, destruction of normal renal tissue and extension into surrounding
areas. Treatment is by percutaneous drainage. This should only he performed with adequate
antibiotic cover and a minimum of manipul ation, 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 lime, particularly
in the elderly, and may then be associated with cortical loss and perinephric disease (Fig.
3038).

Xanthogranulomatous pyelonephritis This is a chronic i nflammatory 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 are thought to provoke mild
impairment of drainage, which initiates and propagates the disease. The infecting organism is
usually E. coli o Proteus mirabilis. There is a marked female preponderance and 1 0 (/( of
patients are diabetic. 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 tumour (tumefactive
xanthogranulomatous pyelonephritis) but ultimately there is renal atrophy, which may be
marked. Ultrasound and CT show loss of normal corticomedullary differentiation and
heterogeneity, which includes debris-containing cystic areas and calculi. The disease usually
extends into the perinephric space with obliteration of tissue planes on all modalities (Fig.
30.39). With further extension through the l ayers 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. Enhancing 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.