Keywords
acute pyelonephritis - papillary necrosis - pyonephrosis - renal abscess
Introduction
Acute renal infection or acute pyelonephritis (AP) denotes the process of inflammation
of the renal parenchyma and its collecting system and the urothelium following infection.
Uncomplicated AP commonly affects otherwise healthy, young women without structural
or functional urinary tract abnormalities and without relevant comorbidities. More
severe and complicated AP occurs in patients with a structurally or functionally abnormal
genitourinary tract, or in persons with a predisposing medical condition like immune
compromised state and diabetes. Complicated AP is characterized by a broader spectrum
of clinical presentations, a wider variety of infecting organisms, and a greater risk
of progression to a complication, such as intrarenal or perinephric abscess or emphysematous
pyelonephritis[1] and has the capacity to damage the organ and at times maybe life threatening. As
histological specimens are difficult to obtain, clinical correlation with stages of
inflammation and developing complication is nearly impossible. In day-to-day clinical
practice, the primary goal of imaging is to provide information about the nature and
extent of the disease and to identify significant complications, for example, gas-forming
infection, abscess, and urinary obstruction.[2]
Ultrasonography (USG) is the most widely used screening tool, although it is limited
in its ability to map disease progression and suffers from operator bias. Currently,
computed tomography (CT) with or without CT urography and magnetic resonance imaging
(MRI) find wide acceptance for diagnosis of AP and its potential complications. This
article attempts to discuss the pathophysiology of AP from the standpoint of medical
imaging and also brings out illustrative examples of various manifestations of AP
and its complications. It provides imaging insight into various stages of inflammation,
development of complication, and a roadmap for understanding AP through cross-sectional
imaging.
Acute Pyelonephritis: Terminological Conundrum
Acute Pyelonephritis: Terminological Conundrum
Numerous verbal expressions have added to the confusion about the terminology used
to describe the extent and severity of AP. Popular terminology used by radiologists
was based solely on imaging appearance without histological confirmation. The advanced
generalized form of AP in diabetic patients, usually with a nonfunctioning kidney
on excretory urography, was originally described as acute bacterial pyelonephritis.[3] The localized form of AP resulting in a mass-like appearance in imaging studies
was given numerous names including acute focal pyelonephritis, acute focal bacterial
nephritis, and acute lobar nephronia[4]
[5] ([Fig. 1]).
Fig. 1 (A) Axial and sagittal (B) CT sections in the nephrographic phase of a 52-year-old diabetic man show round
mass like areas of reduced enhancement representing lobar nephronia (arrows).
As cross-sectional modalities have evolved, subtle abnormal nephrographic findings
were picked up variably termed as cellulitis, carbuncle, and renal phlegmon. In 1984,
Talner et al[6] proposed that all renal parenchymal abnormalities without formation of abscess attributable
to acute infection maybe called AP. It was proposed that degree of involvement should
be described by one or more of the following modifiers: (1) unilateral or bilateral,
(2) focal or diffuse, (3) focal swelling or no focal swelling, and (4) renal enlargement
or none.
Acute Pyelonephritis: Must Know Clinical Issues
Acute Pyelonephritis: Must Know Clinical Issues
Clinically AP is suggested by flank pain, nausea, and vomiting, fever (>38°C), or
costovertebral angle tenderness, and it can occur in the absence of symptoms of cystitis.[7]
AP in pregnant women may not only develop into renal and respiratory insufficiency,
but also there is added risk of frequent preterm labor.[8] It is of great importance to diagnose AP confidently and pick up complications early
to provide effective treatment. Most men with febrile urinary tract infection (UTI)
develop concomitant prostatitis.[9] Prostate infections are notoriously difficult to cure and need long-term antibiotics.
A diagnosis of AP in a man should remind us to image the prostate, preferably by transrectal
USG or a diffusion-weighted MRI (DWI). Diabetic patients with AP are at risk of developing
hypo- and hyperglycemia, hyperosmolar dehydration, or ketoacidosis[10] and also infection by gas-forming organisms with a high mortality (emphysematous
pyelonephritis). Emphysematous pyelonephritis is characterized histologically by acute
pyogenic infiltration with microabscesses and the development of acute renal failure.[11] Laboratory findings of AP include urinary pus cells in excess, granular or leukocytic
casts, bacteriuria, and a positive urine culture. Blood tests may show leukocytosis
with a neutrophilic shift, elevated erythrocyte sedimentation rate, elevated C-reactive
protein levels, and occasionally positive blood cultures that grow the same organism
as cultured from the urine.
Acute Pyelonephritis: Pathology and Pathogenesis
Acute Pyelonephritis: Pathology and Pathogenesis
The heralding event is inoculation of the urinary bladder with an infectious organism,
which then migrates up the ureter to the central collecting system. Vesicoureteral
reflux (VUR) is the retrograde flow of urine from the bladder into the ureter and
toward the kidney secondary to a dysfunctional vesicoureteric junction (VUJ). The
VUJ normally acts as a one-way valve, allowing urine flow from the ureter into the
bladder and closing during micturition, preventing back flow. Shorter intramural submucosal
segment of distal ureter increases the likelihood of VUR. The ratio of ureteric submucosal
tunnel length and ureteric diameter critically determines the valve action. In healthy
individual, the ratio is 5:1, while in most patients with primary VUR, it is ~1.4:1.
The ascent of infection from bladder to kidney occurs even in the absence of VUR,
owing to special virulence properties of the bacteria such as the adhesin P fimbriae
and endotoxins. The bacterial endotoxins are believed to inhibit ureteral peristalsis
by inhibiting the adrenergic nerves that supply the smooth muscle of the ureter. The
ureter as a result lays flaccid creating a functional obstruction and urinary stasis.
The ureteric obstruction compromises the forward flow of urine, which is a normal
protective mechanism against upper UTI. Infection originates from the lower urinary
tract and ascends via subepithelial lymphatic channels or directly via the ureter.
Escherichia coli (E. coli) is the most common pathogen. In elderly patients with a history of instrumentation,
however, Proteus mirabilis is a frequent offender. E. coli has the ability to attach to urothelial surfaces via pili or fimbriae. Once the kidneys
are infected there is either global renal enlargement or sometimes there is patchy
areas of inflammation in different stages. Typically, the pelvicalyceal system is
involved first (pyelitis). The renal interstitial inflammation starts from the medullary
region toward the cortex. Hematogenous infection occurs less commonly, where the renal
cortex is involved first.
Complications of AP include abscess formation and spread of infection to perirenal
space and beyond.
Imaging of Acute Pyelonephritis and Its Complications
Imaging of Acute Pyelonephritis and Its Complications
When Do You Image Acute Renal Infection?
Mostly UTIs are treated without imaging as the diagnosis is straightforward. In confounding
situations where significant clinical remissions are not seen following antibiotic
therapy of 3 days, imaging is called for.[12]
[13] In the situation when a definite diagnosis of AP is not established or when patients
present with recurrent episodes of infection, renal imaging is indicated because there
is more likelihood of stones, obstruction, abscess, or a congenital anomaly.
Imaging is also requested in a select group of patients where risk of complications
runs high.
Patients with poorly controlled diabetes mellitus, acquired immunodeficiency syndrome,
renal transplantation, or other immunocompromised disease states are considered at
risk of developing a complicated UTI, including development of renal or perinephric
abscess. Therefore, imaging may be required when such patients present initially.[14]
[15] Special mention must be made about the case of diabetes. Apart from risk of abscess
formation and extrarenal infection spread, diabetics warrant early imaging in UTI.
Up to 50% may not have the typical flank tenderness that helps to differentiate AP
from a lower UTI. Absence of flank pain in diabetics might be a critical confounding
factor and vigil against missing the narrow window of opportunity to initiate early
treatment must be kept.[12]
[16]
Role of Ultrasonography in Acute Pyelonephritis
USG is one of the first imaging investigations to be ordered because it is easily
available and gives a quick look helping to rule out any predisposing factors like
obstruction as well as intra or perirenal collections. However, signs of early AP
may not be visible on USG and mild swelling as well as loss of corticomedullary differentiation
present in such cases is subjective and may be missed.
A large study from South India on role of emergency ultrasound screening (EUS) in
the evaluation of 1,218 patients with clinically suspected AP found that nearly 49%
had a normal EUS, while 51% had at least one major or minor abnormality. The frequency
of hydroureteronephrosis, renal calculi emphysematous changes, and renal abscess was
19.1, 8.9, 2.1, and 1.9%, respectively. Only 5.9% patients required emergency percutaneous
nephrostomy or drainage of an abscess. They concluded that a large proportion of AP
patients has only normal or minor abnormalities and do not need additional screening
and intervention.[17]
CT versus MRI—How Do You Image Acute Pyelonephritis?
The American College of Radiology appropriateness criteria for AP (revised 2018) state
that CT abdomen and pelvis with IV contrast or CT abdomen and pelvis without and with
intravenous (IV) contrast are usually appropriate for imaging complicated patients
in the setting of AP.[18] It also considers imaging investigation as “usually not appropriate” in uncomplicated
cases. CT is a sensitive tool for AP and its sequelae, and it also provides a global
assessment of the abdomen for coincidental pathology. Renal obstruction by urolithiasis
is well picked up by CT apart from its ability to provide superior anatomic detail
for underlying congenital, as well as acquired renal abnormalities.[19]
Ability of contrast-enhanced CT to predict parenchymal changes, change in renal perfusion,
and function are useful predictors of clinical outcome. Studies comparing CT with
USG conclude that additional benefit of CT lies in its ability to detect parenchymal
abnormalities in patients with AP that are generally missed by USG[19]
[20] CT scores over MRI in its ability to detect calculi and gas in pyelonephritis. Soulen
et al[13] emphasized validity of waiting for 72 hours prior to obtaining CT in patients with
AP. In their series, 95% of patients with uncomplicated AP became afebrile within
48 hours of appropriate antibiotic therapy, and nearly 100% did so within 72 hours.
In situations where use of iodinated contrast material must be avoided, MRI is fast
emerging as an alternative to CT in imaging AP.
Role of DWI
In biological tissues that are highly cellular (such as tumors), the higher density
of cell membranes restricts the diffusion of water protons. This restriction to diffusion
manifests as high signal intensity on DWI and corresponding lower apparent diffusion
coefficient (ADC). Use of ADC can serve as a noninvasive sensitive marker for renal
fibrosis as an apparent decrease in ADC is associated with increased number of fibroblasts.
Currently, it has been first author's institutional practice to obtain DWI in situations
where use of IV contrast is risky in diabetics with borderline glomerular filtration
rate, pregnant women suspected of UTI, children with UTI showing prolonged fever and
not responding to treatment. Comparison of DWI versus contrast-enhanced MRI was done
for pediatric population with equivalent outcome for both techniques.[21] Rathod et al did a prospective study with DWI in a series of cases and found a higher
sensitivity of DWI (95%) compared with noncontrast CT (67%) and contrast-enhanced
CT (88%) in the diagnosis of AP. Areas of AP show significantly lower ADC values than
normal renal cortical parenchyma. Renal abscesses show significantly lower ADC values
than areas of AP.[22] Similar observations of high sensitivity, specificity, and accuracy (each at 95%)
with DWI in uncomplicated AP were reported by other studies too.[23] Another exciting application of DWI is that of differentiation of pyonephrosis from
hydronephrosis. Low ADC values of pyonephrosis debris were found particularly helpful
for pregnant patients in the second and third trimesters who may have physiological
hydronephrosis due to compression by the gravid uterus by Chan et al.[24] Prediction of renal function by DWI is found to be a reproducible technique by Thoeny
et al.[25]
CT Protocol for Acute Pyelonephritis
CT Protocol for Acute Pyelonephritis
Craig et al[19] and Stunell et al[26] have studied pyelonephritis by only precontrast and nephrographic phase CT in cases
where obstruction is not suspected. Taniguchi et al[27] reported that scans using only the nephrographic phase had high accuracy with triphasic
scans (which also included precontrast and excretory phases) for the diagnosis of
AP and urolithiasis. This study reported an accuracy of nephrographic phase only CT
of 90 to 92% in the diagnosis of AP and CT of 96 to 99% in the diagnosis of urolithiasis.
Currently in our institutions, we justify use of unenhanced CT for detecting calculi,
gas-forming infections, and hemorrhage. First and second authors institutional protocol
includes a nephrographic phase at 60 to 90 seconds and excretory phase at 5 to 10
minutes post IV contrast injection studies to completely evaluate patients with renal
inflammatory disease and also to define changes in the renal excretion of the contrast
material that occur as a result of the inflammation. Papillary necrosis that is not
uncommon is also better evaluated in the excretory phase. Our current experience also
dictates that certain findings like streaky nephrogram, delayed parenchymal enhancement,
and urothelial thickening are well picked up in excretory phase images.
Second author's institutional protocol additionally includes a corticomedullary phase
at 25 to 30 seconds post-IV contrast injection to cover any vascular complications
like pseudoaneurysms, preoperative arterial mapping if any surgical intervention is
required and assessing incidentally detected cysts and masses ([Fig. 2]).
Fig. 2 A 68-year-old nondiabetic man with AP. Panels A (coronal) and B (axial) in the corticomedullary or arterial phase show an incidentally detected small
renal cell carcinoma (arrows) that was not picked up by ultrasonography possibly because
of adjacent architectural changes and heterogeneity caused by the AP. Panels C (coronal) and D (axial) in the nephrographic phase show that the mass is isodense to the parenchyma
(arrows) and difficult to identify highlighting the importance of the corticomedullary
phase.
MRI Protocol for Acute Pyelonephritis
MRI Protocol for Acute Pyelonephritis
At First author's institution, DWI is used with multiple b values (–50, 600, 1,000).
The protocol includes fat-saturated T2 in axial and T2 coronal, axial, and coronal
LAVA (which gives in and opposed phase images, Water LAVA T1, Fat LAVA T1) and in
most cases axial and coronal FS T1 following IV Gadolinium.
Imaging Findings of Acute Pyelonephritis: Illustrative Cases
Imaging Findings of Acute Pyelonephritis: Illustrative Cases
In first author's institutional experience of over two decades and retrospective analysis
of 100 cases of AP, the commonest imaging findings were global renal swelling (88%),
perirenal fascial thickening (76%), perinephric fat stranding (56%), streaky nephrogram
(44%), frank abscess (44%), microabscess (32%), gas in renal collecting system or
parenchyma suggestive of emphysematous infection (16%), and abdominal wall involvement
(8%).
Streaky Nephrogram
The common CT finding of striated or streaky nephrogram ([Fig. 3]) is seen as linear bands of alternating hyper- and hypoattenuation orientated parallel
to the axis of the tubules and collecting ducts. After administration of contrast
material, this pattern of differential enhancement reflects the underlying pathophysiology
of tubular obstruction caused by inflammatory debris within the lumen, interstitial
edema, and vasospasm. All three of these pathophysiologic disturbances tend to decrease
the flow of contrast agent through the renal tubule, which also helps explain the
pattern of delayed and persistent enhancement seen 3 to 6 hours after administration
of contrast material. The sites that originally demonstrated reduced attenuation during
the nephrographic phase transmute from hypoattenuation to hyperattenuation wedge-shaped
defects because of the prolonged accumulation of contrast agent that slowly transits
the compromised tubules. The learning point here is that though a streaky nephrogram
is taught to be associated with AP, it is also common to be seen in case of renal
vein thrombosis and acute renal or ureteric obstruction. Visualization of a thrombus
in the renal vein and an anatomical obstruction or calculi in the ureter are not difficult
to pick up on CT. In our experience, streaky nephrogram or hypoperfused areas may
not be well seen in initial nephrographic phase in some situations, but may be better
depicted in narrow window settings in the excretory phase images ([Figs. 4A]
[C]
[5A]
[B]).
Fig. 3 A young woman presenting with fever with chill and rigor, dysuria, and increased
frequency. Nephrographic phase axial CT shows alternating bands of hypo- and hyperattenuation
in both the kidneys in panel (A) and patchy enhancement with alternate hypo- and hyperattenuation
areas in left kidney (B).
Fig. 4 Near normal nephrographic phase axial CT image (A). In narrow window setting the heterogenous parenchymal enhancement is depicted in
a delayed phase axial CT image (B). Complimentary diffusion-weighted imaging was done that reveals a dramatic appearance
of alternate bright and hypointense areas suggesting restricted diffusion in renal
parenchyma paralleling heterogenous enhancement seen in CT.
Fig. 5 (A and B) Axial CT sections: Initial nephrographic phase image (A) fails to depict patchy parenchymal enhancement of kidneys that is depicted in 10
minutes excretory phase images (B). Note can be made of perinephric fat stranding around left kidney and urothelial
thickening of left renal pelvis.
Renal Swelling
The finding of renal swelling is best assessed by experience rather than measurement
([Fig. 6]). Although renal swelling is a common feature, not all cases of AP present with
swollen kidney. Perinephric fat stranding and perirenal fascial thickening are also
found by the authors to be contributory but nonspecific findings.
Fig. 6 Coronal axial CT section in the nephrographic phase in a 23-year-old man reveals
a significantly swollen left kidney with reduced enhancement (arrow).
Renal Microabscesses
Small microabscesses are seen in almost a third of cases of AP. These may coalesce
and form larger abscesses and are well picked up by both CT and DWI ([Figs. 7]
[8]).
Fig. 7 (A) An axial CT reveals swollen kidney with small microabscesses (straight arrow), perirenal
fascial thickening (elbow arrow), and dirty fat around kidney suggesting inflammation.
(B) In a different case, microabscesses are (C) showing restricted diffusion in diffusion-weighted magnetic resonance imaging seen
as hyperintense areas with corresponding lowered apparent diffusion coefficient (ADC)
(arrow) in affected renal parenchyma. ADC value of inflamed parenchyma in right kidney
measures 0.93 × 10–3 mm2/sec to 0.95 × 10–3 mm2/s and in contralateral normal left kidney, it is 2.0 × 10–3 mm2/s.
Fig. 8 Panels A (axial) and B (sagittal) CT sections in a 68-year-old diabetic woman reveal clusters of tiny cysts
representing microabscesses (straight arrows). Coalescing microabscesses evolving
into a larger abscess are also seen (elbow arrow)
Urothelial Thickening
Subtle urothelial thickening and increased urothelial enhancement in the walls of
the renal pelvis as well as the ureter and along the mucosal layer of the urinary
bladder can be well seen on CT and aid the diagnosis of AP especially in cases where
renal changes are mild ([Fig. 9]).
Fig. 9 Curved sagittal CT reconstruction in the nephrographic phase through the right kidney
and ureter of a 51-year-old diabetic woman show mild diffuse urothelial thickening
and increased enhancement of the renal pelvis and ureter (arrow).
Renal Abscess
Renal abscess is a relatively rare consequence of treated cases of AP. But in poorly
treated or inappropriately treated cases and in immunocompromised, especially in diabetics,
renal abscess is a relatively frequent unwanted consequence. Hematogenous infections
cause multiple abscesses ([Fig. 10]). CT is the modality of choice showing intrarenal loculations as well as extrarenal
extent. There is excellent depiction of pus by DWI ([Figs. 7B]
[C]), which can be performed for patients who are unfit for contrast CT or where radiation
exposure is a concern like in pregnant women and children. On CT renal parenchyma
around the abscess cavity may appear poorly enhanced on the nephrogram phase due to
edema. This hypoattenuating subjacent renal parenchyma may enhance slowly in delayed
images excluding necrosis ([Fig. 11A]). Multiple abscesses may be seen where septic emboli seed the kidney. Presence of
air within the abscesses, collecting system, and the parenchyma is a sign of fulminant
infection and called emphysematous pyelonephritis. This will be dealt in the upcoming
part 2 of our article ([Fig. 11B]).
Fig. 10 (A) Axial nephrographic CT section in a 56-year-old diabetic man reveals a thick-walled
abscess with surrounding hypoperfused parenchyma. (B) Diffusion-weighted magnetic resonance imaging reveals restricted diffusion and low
apparent diffusion coefficient 0.71 × 10–3 mm/ (C).
Fig. 11 Coronal nephrographic CT through the right kidney in a 25-year-old woman reveals
two abscesses (star) and the perifocal edema around them (straight arrows). Subtle
urothelial thickening and enhancement are also seen (elbow arrow)
Postinflammatory Noninfected Fluid Collections
Postinflammatory cystic fluid collection may develop in an area of AP during or after
antibiotic treatment ([Fig. 12A]
[B]). Renal abscess needs to be differentiated from postinfective sterile fluid collections
that are sometimes seen following effective treatment. The principal differentiating
point between renal abscess and postinflammatory sterile fluid is enumerated in [Table 1].
Fig. 12 Axial nephrographic CT sections in a 55-year-old man showing post-infective fluid
collection without enhancing wall or hypoperfused surrounding parenchyma (A) and in another 36-year-old woman showing right renal abscess with hypoperfusion
of perifocal parenchyma and extensive perinephric fat stranding signifying acute pathology
(B).
Table 1
Differentiating postinflammatory fluid and renal abscess
|
Postinflammatory sterile fluid
|
Renal abscess
|
|
Abbreviations: MRI, magnetic resonance imaging; USG, ultrasonography.
|
-
<3 cm in diameter
-
No wall thickening or enhancement
-
Perinephric fat remains clean
-
Aspiration shows brownish fluid
-
USG reveals anechoic fluid without debris
-
No diffusion restriction in MRI
|
-
No size criteria
-
Wall thickening and enhancement
-
Perinephric fat stranding common
-
Aspiration reveals pus
-
USG reveals debris
-
Restricted diffusion in MRI
|
Extrarenal Extension of Abscess
Spread of renal infection to perinephric spaces following abscess rupture is not uncommon.
Abscess may extend to involve the perinephric spaces, the posterior abdominal wall,
or psoas muscle ([Fig. 13A]
[B]).
Fig. 13 (A) Axial nephrographic CT in a 64-year-old diabetic man with poor glycemic control
shows a large renal abscess with perinephric extension of inflammation. (B) Axial nephrographic CT in another 62-year-old diabetic woman shows a subcapsular
rupture of the abscess in the left kidney with extension into posterior abdominal
wall (elbow arrow) and left psoas muscle (straight arrow).
Obstructing Pathology
Presence of obstructing calculus is a risk factor for developing infection. Obstruction
of ureter causes increased tissue pressure in kidney that in turn impedes microcirculation
and that leads to reduced ability to clear infection. It is important to image the
urinary tract for any calculi, ureteric stricture, or mass that predisposes to urinary
stasis and subsequent pyelonephritis ([Figs. 14]
[15]
[16]).
Fig. 14 Coronal (A) and axial (B) nephrographic CT image of left kidney of a 43-year-old man with obstructed renal
collecting system by ureteric calculi (long arrows). There is infection in the upper
pole with abscess formation (short arrow)
Fig. 15 Coronal oblique CT volume rendered nephrographic phase (A), maximum intensity projection excretory phase (B), and diagrammatic representation (C) through the right kidney and ureter of a 29-year-old man with acute pyelonephritis
show a retrocaval ureter (curved arrows) causing hydronephrosis. The inferior vena
cava is marked with a star. The straight arrow in panel A shows urothelial thickening
of the pelvic wall signifying infection.
Fig. 16 Sagittal curved CT reconstruction in the nephrographic phase (A) and diagrammatic representation (B) through the left kidney, ureter, and bladder in a 33-year-old lady with acute pyelonephritis
and hydronephrosis show a ureterocele (long arrow) as the cause of the obstruction.
The upper pole of the kidney reveals a poorly enhancing area suggestive of infection
(short stout arrow). Three loose lying nonobstructive calculi are seen in the distal
dilated ureter (elbow arrows).
Pyonephrosis
Pyonephrosis meaning pus within the collecting system is a situation where obstructed
dilated collecting system is laden with pus. USG depiction of debris within a dilated
collecting system or documentation of diffusion restriction in MRI helps to establish
diagnosis. CT may detect thickened walls of the renal pelvis and ureter, hyperdense
urine within the collecting system suggestive of debris, fluid-fluid levels (pus-urine,
urine-debris, or contrast-debris levels), and gas within the collecting system to
contribute to a diagnosis ([Fig. 17]).
Fig. 17 Oblique coronal CT reconstruction in the nephrographic phase through the left kidney
and ureter of a 78-year-old man with chronic left ureteric obstruction by calculi
(short arrow). The urine reveals high density (25 HU) suggestive of debris signifying
a diagnosis of pyonephrosis. An abscess is seen leading from one of the posterior
calyces into the abdominal wall muscles at the back (long arrow).
Infected Renal Cysts
Infected renal cysts cannot be reliably differentiated radiologically from an abscess.[28]
[29] An infected cyst may also mimic a renal cyst complicated by intracystic hemorrhage
on imaging studies. Percutaneous cyst aspiration and drainage under CT or US guidance
may be indicated for diagnosis and treatment.
Papillary Necrosis
AP is one of several diseases such as diabetes, analgesic overuse, sickle cell disease,
renal vein thrombosis, tuberculosis, and obstructive uropathy that cause renal papillary
necrosis.[30] CT findings include contrast filled clefts in the renal medulla in the excretory
phase, nonenhanced lesions surrounded by rings of excreted contrast material representing
sloughed off medullae, and medullary calcifications. Sloughed off papillae may also
be seen in the renal pelvis or ureter and may cause ureteric obstruction ([Fig. 18]).
Fig. 18 Sagittal CT maximum intensity (A), volume rendered (B), and colored volume rendered (C) images through the left kidney in the excretory phase of a 50-year-old diabetic
woman with acute pyelonephritis show deformed ballooned calyces with filling defects
(straight arrows) along with medullary clefts and deformities of the calyces (curved
arrows). A minimum intensity projection through the right kidney in the plain scan
(D) of another 68-year-old man with deranged renal functions shows pelvicalyceal mild
dilatation along with clubbing and deformity of several calyces (curved arrows).
An imaging algorithm for patients with AP has been provided in [Fig. 19]
Fig. 19 Acute pyelonephritis imaging approach. AP, acute pyelonephritis; CT, computed tomography.
Conclusion
Early detection of AP is important to avoid complications especially in vulnerable
groups of patients. A USG helps to rule out obstruction in most patients. CT helps
in patients who have complicated AP, have not responded to treatment, or are very
sick. The sensitivity and specificity of CT for early detection of AP and mapping
extra renal extent of disease process are high. MRI is reserved for patients where
CT is contraindicated.
