Atypical Low-Signal-Intensity Renal Parenchyma: Causes and

EDUCATION EXHIBIT
833
RadioGraphics
Atypical Low-SignalIntensity Renal
Parenchyma: Causes
and Patterns1
CME FEATURE
See accompanying
test at http://
www.rsna.org
/education
/rg_cme.html
LEARNING
OBJECTIVES
FOR TEST 4
After reading this
article and taking
the test, the reader
will be able to:
䡲 List the spectrum
of renal diseases that
cause low signal intensity on T2weighted MR images.
䡲 Describe the
pathophysiologic
mechanism of low
signal intensity on
T2-weighted MR
images.
䡲 Recognize the MR
imaging findings of
each renal disease
that causes low signal
intensity.
Jun Yong Jeong, MD ● Seung Hyup Kim, MD ● Hak Jong Lee, MD
Jung Suk Sim, MD
Certain renal diseases manifest as low signal intensity of the renal parenchyma on magnetic resonance images. Sometimes, the appearance
is sufficiently characteristic to allow a specific radiologic diagnosis to be
made. The causes of this finding can be classified into three main categories on the basis of the pathophysiology: hemolysis, infection, and
vascular disease. The first category includes paroxysmal nocturnal hemoglobinuria (PNH), hemosiderin deposition in the renal cortex from
mechanical hemolysis, and sickle cell disease. The second category includes hemorrhagic fever with renal syndrome (HFRS). The third category includes acute renal vein thrombosis, renal cortical necrosis, renal arterial infarction, rejection of a transplanted kidney, and acute
nonmyoglobinuric renal failure with severe loin pain and patchy renal
vasoconstriction. These disease processes have different patterns of low
signal intensity. PNH, hemosiderin deposition from mechanical hemolysis, and sickle cell disease involve the entire cortex including the columns of Bertin. HFRS involves the medulla, especially the outer medulla, whereas cortical necrosis involves the inner cortex including the
columns of Bertin. In renal vein thrombosis, low-signal-intensity lesions involve the outer medulla, an appearance resembling that of
HFRS. Wedge-shaped low-signal-intensity regions involving both the
cortex and the medulla are seen in arterial infarction.
©
RSNA, 2002
Abbreviations: HFRS ⫽ hemorrhagic fever with renal syndrome, PNH ⫽ paroxysmal nocturnal hemoglobinuria
Index terms: Hemorrhagic fever, 811.659 ● Kidney, diseases, 811.65 ● Kidney, infarction, 811.77 ● Kidney, necrosis, 811.654 ● Renal veins, thrombosis, 811.751 ● Sickle cell disease (SS, SC), 811.651
RadioGraphics 2002; 22:833– 846
1From
the Department of Radiology and Institute of Radiation Medicine, Seoul National University College of Medicine, 28 Yongon-dong, Chongno-gu, Seoul 110-744, Korea; and the Clinical Research Institute, Seoul National University Hospital. Presented as an education exhibit at the 2000
RSNA scientific assembly. Received June 8, 2001; revision requested July 17; final revision received February 12, 2002; accepted February 28. Supported in
part by the 2000 BK21 Project for Medicine, Dentistry, and Pharmacy. Address correspondence to S.H.K. (e-mail: [email protected]).
©
RSNA, 2002
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Introduction
Although intravenous urography, ultrasonography (US) with Doppler imaging, and computed
tomography (CT) remain the primary imaging
modalities for evaluation of the kidney, magnetic
resonance (MR) imaging may provide additional
information that can lead to a better understanding of the changes in the renal parenchyma in
some disease processes.
In normal, well-hydrated kidneys, the renal
cortex has a shorter T1 than the medulla and
therefore appears more intense than the medulla
on T1-weighted MR images (1). The loss of this
normal corticomedullary differentiation is a nonspecific finding that may be seen in a variety of
renal disorders in which the cortex and the medulla appear isointense (2). Loss of signal intensity of the renal parenchyma on T2-weighted images is unusual but can be a relatively specific feature at MR imaging. Usually, low signal intensity
is caused by calcification or ossification, hypercellularity with scant cytoplasm, fibrocollagenous
stroma, high-protein material, paramagnetic substances such as melanin, free radicals, and hemorrhage (3). The low signal intensity in most of
these conditions is based on the fact that there is
little free hydrogen ion in the lesion or on the
paramagnetic properties of the deposited substances.
The patterns of signal intensity changes in
hemorrhage are complex. Generally, the paramagnetic properties of iron alter the usual signal
intensity characteristics of tissue. Recognition of
iron within an organ is necessary for accurate differential diagnosis with MR imaging (4,5). When
blood extravasates into tissue, oxyhemoglobin
molecules within the red blood cells lose oxygen,
becoming deoxyhemoglobin. Within a few days,
the ferrous (Fe2⫹) iron in hemoglobin converts
into ferric (Fe3⫹) iron, forming methemoglobin,
which cannot carry oxygen. Subsequently, methemoglobin is digested by macrophages and the
iron is ultimately stored as hemosiderin. Each of
these iron-containing substances has different
magnetic properties that affect its appearance on
MR images. Deoxyhemoglobin and methemoglobin are paramagnetic, hemosiderin is superparamagnetic, whereas oxyhemoglobin is diamagnetic, having no paramagnetic effect (5–7). They
result in signal intensity changes at T1- and T2weighted MR imaging that can facilitate or complicate diagnosis of renal lesions.
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Hemosiderin has paramagnetic effects and
shortens predominantly T1 and T2 relaxation
times at low and high concentrations, respectively
(8,9). At low concentrations, T1 shortening is
maximal; it may appear as slightly increased signal intensity on T1-weighted images and decreased signal intensity on T2-weighted images. A
higher concentration of hemosiderin dramatically
decreases T2. Because T1-weighted images are
influenced by changes in T2 as well as in T1, signal intensity can be decreased on T1-weighted
images as well. Therefore, the appearance of hemosiderin on T1-weighted images varies; it may
appear as minimally increased signal intensity, as
loss of corticomedullary differentiation, or as
marked low signal intensity, depending on the
amount of hemosiderin deposition. T2-weighted
images are more sensitive than T1-weighted images for detection of hemosiderin (10 –12). Moreover, Tanaka et al (11) concluded that T2*weighted imaging is superior to T2-weighted imaging in detection of renal cortical hemosiderosis
because of the higher magnetic susceptibility effect and shorter examination times.
The diseases that cause low signal intensity of
the renal parenchyma on MR images can be divided into three main categories on the basis of
the pathophysiology: hemolysis, infection, and
vascular disease. The first category includes paroxysmal nocturnal hemoglobinuria (PNH), hemosiderin deposition in the renal cortex by mechanical hemolysis, and sickle cell disease. The
second category includes hemorrhagic fever with
renal syndrome (HFRS). The third category includes acute renal vein thrombosis, renal cortical
necrosis, renal arterial infarction, rejection of a
transplanted kidney, and acute nonmyoglobinuric
renal failure with severe loin pain and patchy renal vasoconstriction.
Familiarity with the spectrum of findings in the
renal parenchyma resulting from hemorrhage and
iron deposition is necessary for diagnosis and better understanding of the pathogenesis of these
renal diseases (13).
We have obtained spin-echo or turbo spinecho MR images (SPECTRO-20000 2.0 T
[Goldstar Medical Systems, Seoul, Korea] or
Signa 1.5 T [GE Medical Systems, Milwaukee,
Wis]). The repetition time (msec)/echo time
(msec) value was 500–700/20 –30 for T1-weighted
images and 2,000 –2,500/60 – 85 for T2-weighted
images. Gadopentetate dimeglumine (Magnevist
[Schering, Berlin, Germany]; 0.1 mmol/kg) was
used as a contrast medium for enhanced T1weighted images.
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Figure 1. PNH. (a) Axial T1-weighted MR image (500/30) obtained at 2.0 T shows that the signal intensity of the
renal cortex is lower than that of the medulla, causing reversed corticomedullary differentiation. (b) Axial T2weighted MR image (2,000/80) obtained at 2.0 T shows that the signal intensity of the renal medulla is normal, although that of the cortex remains low. Note the abnormal corticomedullary differentiation. (c) Nonenhanced CT
scan shows slight increased attenuation of the renal cortex compared with that of the medulla, making corticomedullary differentiation possible. (d) High-power photomicrograph (original magnification, ⫻400; hematoxylin-eosin
stain) of a biopsy specimen from the kidney shows numerous brownish hemosiderin granules scattered in the tubular
epithelial cells.
Low Signal Intensity Caused by Hemolysis
Paroxysmal Nocturnal Hemoglobinuria
PNH is an acquired myelodysplastic, hematopoietic stem cell disorder caused by an increased sensitivity to complement, resulting in acute or
chronic intravascular hemolysis. Factors that have
been reported to precipitate hemolysis include
infections, reactions to drugs and immunizations,
transfusion, surgery, and exercise; frequently, the
cause remains unknown (10,14). Major clinical
features include hemoglobinuria, iron deficiency
anemia, bleeding, and venous thrombosis (15).
PNH can cause chronic renal failure as a result of
microinfarctions due to repeated episodes of microvascular thrombosis rather than to the tubular
damage from hemosiderin deposition (14) or a
direct nephrotoxic effect of iron (16). The disease
occurs predominantly in adults and is rare in children and adolescents, in whom the prognosis is
worse. The typical histologic finding in the kidney
is deposition of hemosiderin in epithelial cells of
the proximal convoluted tubules in the renal cortex (Fig 1d) (14).
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Figure 2. Intravascular hemolysis due to a prosthetic cardiac valve. (a) Axial T1-weighted MR image (550/30) obtained at 2.0 T shows that the signal intensity of the renal cortex is lower than that of the medulla. (b) Axial T2weighted MR image (2,000/80) obtained at 2.0 T shows that the renal cortex has lower signal intensity than the medulla. (Reprinted, with permission, from reference 18.)
MR imaging is the best imaging modality for
demonstrating hemosiderin deposition in the renal cortex (12). Visual comparison of the signal
intensity of lesions with that of the paraspinous
musculature has been reported to be useful in
assessment of parenchymal iron deposition in
other diseases (17). The MR imaging findings of
PNH include low signal intensity in the renal cortex not only with T1- and T2-weighted sequences
(Fig 1a, 1b) but also with gradient-echo and inversion-recovery sequences (10). This is due to
deposition of hemosiderin in the epithelial cells of
the proximal convoluted tubules in the renal cortex (Fig 1d) (12). This low cortical signal intensity is more conspicuous on T2-weighted images
due to the adjacent high-signal-intensity medulla,
which is not affected in PNH and therefore has a
normal high-signal-intensity appearance. Theoretically, gradient-echo imaging has superior sensitivity to spin-echo imaging in detection of hemosiderin because it uses magnetic gradients to
refocus the transverse magnetization. Gradientecho imaging is also faster (11). At nonenhanced
CT, higher attenuation of the renal cortex can be
seen, but it is less conspicuous than at MR imaging (Fig 1c).
Unlike hemolytic disorders such as sickle cell
disease, in which iron from extravascular hemolysis is mainly deposited in the liver and spleen,
PNH and mechanical damage from heart valves
result in intravascular hemolysis sufficient to saturate the plasma haptoglobin with iron. The hemoglobin passes through the glomerulus and is reabsorbed in the proximal tubules and stored as hemosiderin. Intravascular hemolysis does not
result in hemosiderin accumulation elsewhere in
the body (18).
In contrast to other hemolytic anemias such as
sickle cell disease, autoimmune hemolytic anemia, and hereditary spherocytosis, which are
characterized by heavy deposition of iron in the
liver and spleen, PNH usually demonstrates normal iron concentration in the liver and spleen (although patients with PNH who have received
multiple transfusions may have slightly increased
hepatosplenic levels of iron). As a consequence,
decreased signal intensity within the liver and
spleen occurs less often in patients with PNH
than in conditions such as hemochromatosis and
transfusion hemosiderosis or as a consequence of
hepatic or portal vein thrombosis or long-standing biliary cirrhosis (13). In the absence of cortical calcification, diffuse low signal intensity in the
renal cortex indicates intravascular hemolysis
rather than systemic iron overload. When transfusional siderosis is absent, low signal intensity confined to the kidney suggests PNH, whereas low
signal intensity limited to the spleen and liver is
characteristic of transfusional hemosiderosis and
hemochromatosis (19,20).
The MR imaging findings of PNH in the kidney are almost opposite to those seen in HFRS, in
which medullary hemorrhage results in low signal
intensity of the medulla (21).
Hemosiderin Deposition
by Mechanical Hemolysis
Although hemosiderin deposition in the renal cortex by mechanical hemolysis due to a malfunctioning prosthetic cardiac valve has a different
pathogenesis from PNH, the pattern of renal iron
deposition and the MR imaging findings are identical (Fig 2).
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Lee et al (18) reported that the signal intensity
of the renal cortex was much lower than that of
the medulla on T2-weighted images due to deposition of hemosiderin in proximal convoluted tubules by intravascular hemolysis. Although the
incidence is low, mechanical hemolysis due to a
malfunctioning prosthetic cardiac valve should be
included in the differential diagnosis as a possible
cause of low signal intensity of the renal cortex on
T1- and T2-weighted MR images. At MR imaging, PNH is indistinguishable from mechanical
hemolysis (Figs 1, 2) (18). Similarly, any other
cause of intravascular hemolysis such as hemolytic anemia can cause low signal intensity within
the renal cortex due to hemosiderin deposition
(22).
Sickle Cell Disease
Sickle cell disease is a common hereditary disorder in African-Americans. Although sickle cell
disease is primarily a hematologic disorder, several renal syndromes have been referred to as
sickle cell nephropathy (23).
Sickle cell nephropathy is known to involve all
parts of the kidney parenchyma (24). Cortical
changes include dilatation and engorgement of
glomerular capillary tufts, glomerular sclerosis,
increased mesangial matrix, and iron deposition
in the glomerular epithelium secondary to sickled
erythrocytes (24). Although engorgement and
dilatation of capillaries and edema and focal scarring of the papillary stroma associated with dilatation and congestion of peritubular and pelvic mucosal capillaries are the pathologic changes in the
renal medulla, they are not likely to be observed
on MR images (24).
Patients with mild sickle cell disease who have
not undergone transfusion do not develop iron
overload in the renal cortex because extravascular
hemolysis in the reticuloendothelial system (eg,
the spleen) by defective red blood cells is the
main pathophysiology (13,19). However, acute
hemolytic crises or intravascular hemolysis contributes up to one-third of the hemolysis in sickle
cell disease and causes hemosiderin and ferritin
storage in the renal proximal convoluted tubule
(13,19). This explains the low signal intensity of
the renal cortex on T2-weighted MR images (24).
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The MR imaging findings of sickle cell disease
are the same as those of PNH and mechanical
damage from heart valves, although in mild cases
they will not be seen (13,19,24). Differentiating
among the various causes of intravascular hemolysis is impossible with MR imaging (Figs 1, 2)
(13). On T2-weighted MR images, low signal
intensity of the spleen due to extravascular hemolysis is noted in all sickle cell disease patients irrespective of their transfusion history (19). However, low signal intensity of the liver or pancreas
can be seen only in patients who have received
multiple blood transfusions (19).
Renal failure in sickle cell disease is not dependent on iron deposition. When renal failure develops in sickle cell disease, involvement of the renal
glomeruli, distal tubules, or renal medulla and
renal infection are more likely causes (19).
Low Signal Intensity Caused by Infection
HFRS, formerly referred to as Korean hemorrhagic
fever, is an acute infectious, rodent-transmitted
disease caused by the genus Hantavirus and clinically characterized by fever, visceral hemorrhage,
and a variable degree of renal failure. The Seoul
virus and the Hantaan virus are the most important etiologic agents of HFRS in Korea (25).
HFRS occurs primarily in Asia and Europe and is
a major public health problem in Far Eastern
Asia, especially in Korea, where the mortality rate
is 3%–5% (26).
There are five relatively well-defined, successive clinical stages: febrile, hypotensive, oliguric,
diuretic, and convalescent. The renal changes
begin in the hypotensive or oliguric phase and
persist during the diuretic phase (27).
The central derangement of HFRS seems to be
vascular dysfunction (28), but the exact pathophysiologic mechanism is not understood. The
most prominent pathologic features of HFRS are
congestion and hemorrhage with hemorrhage,
hemosiderin formation, and cellular reaction in
the renal medulla, right atrium of the heart, and
anterior lobe of the pituitary gland (Fig 3c, 3d)
(29,30).
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Figure 3. Images of an isolated kidney specimen from a 21-year-old man who died of HFRS. (a) T1-weighted MR
image (500/30) shows that the low-signal-intensity medulla is clearly differentiated from the cortex. (b) T2-weighted
MR image (2,000/80) shows low signal intensity of the whole medulla, resulting in marked abnormal corticomedullary contrast. (c) Photograph of the pathologic specimen shows severe hemorrhage and congestion confined to the
medulla with an intact cortex. (d) Photomicrograph (original magnification, ⫻100; hematoxylin-eosin stain) shows
hemorrhage and intertubular congestion in the medulla, which are the typical microscopic findings of HFRS. Note
that there is no hemorrhage around the glomeruli and proximal tubules. (Reprinted, with permission, from reference 32.)
The congestion and hemorrhage are most
prominent in the outer or subcortical zone of the
medulla and extend deep into the medullary tissues (Figs 3, 4) (30). Microscopic features of the
kidney in HFRS are renal swelling, intense congestion and hemorrhage in the renal medulla, and
acute tubular necrosis (Fig 3d) (27,31).
The low signal intensity is noted in the renal
medulla, either the outer portion or the entire
medulla, irrespective of the clinical phase, on
both T1- and T2-weighted images but is more
prominent on T2-weighted images (Figs 3, 4)
(21). Reversed corticomedullary differentiation
on T2-weighted images (bright cortex, dark medulla) with preserved corticomedullary distinction
on T1-weighted images is another MR imaging
finding (Figs 3a, 4a). These findings are opposite
to those seen in PNH (Fig 1), in which cortical
hemosiderin deposition results in a diminution or
reversal of corticomedullary demarcation on T1weighted images and an enhancement of abnormal
corticomedullary demarcation on T2-weighted
images (8,21).
The most prominent finding at MR imaging, a
well-defined zone of low signal intensity in the
outer medulla, correlates well with the histopathologic findings of HFRS (Fig 3c). The
cause of the low signal intensity of the medulla is
congestion and hemorrhage of the outer medulla
(21). MR images obtained in the oliguric and diuretic phases show various degrees of globular
renal swelling; in the convalescent phase, the kidneys revert to their normal shape (21).
At first, deoxyhemoglobin, intracellular methemoglobin, and hemosiderin are the causes of low
signal intensity on T2-weighted images (6,21,32).
Deoxyhemoglobin is the cause of low signal in-
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Figure 4. Convalescent phase HFRS in a 46-year-old man. (a) Axial T1-weighted MR image (550/30) obtained at
2.0 T shows low signal intensity in the renal medulla and higher signal intensity in the cortex. The low-signal-intensity line (arrows) along the lateral margin of the right kidney is due to chemical shift artifact. (b) Axial T2-weighted
MR image (2,000/80) obtained at 2.0 T shows nearly the same low signal intensity in the outer renal medulla and
high signal intensity in the cortex and inner medulla.
Figure 5. Renal vein thrombosis. (a) Axial T1-weighted MR image (500/30) obtained at 2.0 T shows a swollen
right kidney with diminished corticomedullary contrast. (b) Axial T2-weighted MR image (2,500/100) obtained at
2.0 T shows low signal intensity in the outer part of the medulla. (Reprinted, with permission, from reference 33.)
tensity on T1-weighted images (6,21,32). In addition, after the convalescent phase, persistent
low signal intensity in the medulla in HFRS may
be caused by intertubular fibrosis (6,21,32). The
Seoul variant of the viral infection has less bleeding, vascular changes, and renal derangement but
more severe liver dysfunction than HFRS caused
by the Hantaan variant (25). Accordingly, the
MR imaging findings of HFRS caused by the
Seoul virus may be less conspicuous than those of
HFRS caused by the Hantaan virus (25,32).
Although low signal intensity in the outer medulla at MR imaging may be seen in renal parenchymal changes due to renal vein thrombosis (Fig
5) (33), it is a fairly characteristic MR imaging
feature of HFRS in the appropriate clinical circumstances. MR imaging can be helpful in diagnosis of HFRS, especially in the early phase of
HFRS, when differentiation from other diseases
such as leptospirosis, murine typhus, or scrub
typhus is difficult (21). However, definitive diagnosis depends on serologic tests. MR imaging can
also be used to detect complications of HFRS,
including retroperitoneal hemorrhage and rupture
of the kidney (21).
Low Signal Intensity
Caused by Vascular Disease
Acute Renal Vein Thrombosis
Renal vein thrombosis is most common in patients with membranous glomerulonephritis.
However, there are other predisposing conditions,
including membranoproliferative glomerulonephritis, diabetic nephropathy, lupus nephritis,
amyloidosis, sarcoidosis, sickle cell anemia, transplantation, malignancy, dehydration, and sepsis;
infants of diabetic mothers are also predisposed to
renal vein thrombosis. It is also seen in retroperitoneal malignancies, abdominal tumors, trauma,
hypercoagulable states, and retrograde extension
of a thrombus from the inferior vena cava (34).
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Figure 6. Renal vein thrombosis in a transplanted kidney.
(a) Axial T1-weighted MR image (500/30) obtained at 2.0 T
shows a swollen transplanted kidney with poorly defined low
signal intensity in the medulla. (b) Coronal T1-weighted MR
image (500/30) obtained at 2.0 T shows the same features as
in a. (c) Axial T2-weighted MR image (2,500/100) obtained
at 2.0 T shows prominent areas of low signal intensity in the
renal medulla. (Reprinted, with permission, from reference
33.)
Because the duration of the thrombosis is a
factor in the effectiveness of therapy, it is important to make the diagnosis and to determine the
site of the thrombus as early as possible in the
least invasive manner. However, renal vein
thrombosis can be difficult to diagnose with less
invasive techniques, including excretory urography, US, CT, and radionuclide imaging (35–39).
MR imaging has been suggested as a possible
noninvasive diagnostic modality for deep vein
thrombosis. MR imaging findings in the kidney
with acute renal vein thrombosis include renal
swelling, indistinct corticomedullary differentiation at T1-weighted imaging, and prolongation of
the T1 and T2 relaxation times of the renal cortex
and medulla with resulting low signal intensity
(Figs 5, 6) (36,40). There are additional imaging
findings, such as obliteration of the renal sinus fat
and compression of the renal collecting systems,
marked attenuation of the renal veins, multiple
venous collateral vessels in the perinephric region,
and dilatation of the gonadal vein (35).
In obstruction of the renal vein, the inner part
of the medulla is less involved than the cortex and
the outer part of the medulla because the outer
part of the medulla is especially vulnerable to hypoxic injury (41). A low-signal-intensity band in
the outer part of the medulla was noted in patients with acute renal vein thrombosis, similar to
the findings in patients with HFRS (Figs 3, 4)
(21). The pathologic basis of the low signal inten-
sity in the medulla is nearly the same as that in
HFRS (21).
According to the results of an experimental
study of MR imaging with ligation of the renal vein
to cause acute renal vein thrombosis (33,42,43),
on T1-weighted images, the involved kidney enlarged maximally on the third day and returned to
its initial size within 2 weeks. Decreased signal
intensity of the renal parenchyma was noted on
the first day. On T2-weighted images, four concentric layers of alternating low and high signal
intensity were visualized. In the pathologic specimen, intense congestion and hemorrhage were
found in the medulla—mainly in the outer part—
and the subcapsular cortex (33,42,43). Fibrosis,
hemorrhage, and calcification are contributing
factors to the signal intensity loss on T2-weighted
images (34). The loss of corticomedullary differentiation on T1-weighted images is the first radiologic feature of renal vein thrombosis, appearing
on the first day after the event, and this worsens
over time.
MR imaging can be useful in delineation of the
parenchymal changes associated with renal vein
thrombosis. MR imaging can be considered when
venography is contraindicated or the findings
at other imaging studies such as US or CT are
equivocal (34,44).
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Figures 7, 8. Acute renal cortical necrosis. (7a) Axial T2-weighted MR image (2,000/80) obtained at 2.0 T on the
30th day of renal cortical necrosis shows that both kidneys are shrunken and the low-signal-intensity cortex and columns of Bertin are prominent. The low-signal-intensity line (arrows) along the lateral margin of the right kidney is
due to chemical shift artifact. (7b) Plain radiograph of the kidneys shows diffuse calcification along the cortical margin, which is the cause of the low signal intensity on MR images. (7c) Nonenhanced CT scan shows diffuse calcification involving the renal cortex and the columns of Bertin, which causes the low signal intensity on MR images. (Reprinted, with permission, from reference 45.) (8) In another patient, MR imaging was performed at 1.5 T on the 10th
day after massive upper gastrointestinal bleeding. Contrast-enhanced CT scan of the kidneys shows a nonenhancing
low-attenuation rim with an enhanced outer cortex and medulla.
Renal Cortical Necrosis
Renal cortical necrosis is a rare cause of acute renal failure that is usually associated with thirdtrimester obstetric hemorrhage, particularly abruptio placentae. Other causes of renal cortical
necrosis include severe traumatic shock, septic
shock, transfusion reaction, severe dehydration,
venom toxin, and hemolytic uremic syndrome; it
can also occur as a complication of renal transplantation. Although vasospasm and disseminated intravascular coagulation have been proposed as the primary event causing renal cortical
necrosis, the pathogenesis still remains unclear
(45).
Low signal intensity of the inner renal cortex
and the columns of Bertin with every MR imaging
sequence is the major characteristic finding of
renal cortical necrosis (Fig 7a) (45). Swelling of
both kidneys, corticomedullary differentiation on
T2-weighted images instead of T1-weighted images (Fig 7a), and increased signal intensity of the
cortex on T2-weighted images are other features
of renal cortical necrosis at MR imaging (45).
The area of nonenhanced low signal intensity of
the renal cortex corresponds to the hypoattenuating zone observed on contrast material– enhanced
CT scans (Fig 8) and to the histologic zone of
cortical necrosis (46 – 49).
The thin rim of enhanced subcapsular tissue
on MR images persists because of its separate
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Figure 9. Renal arterial infarction. MR imaging was
performed at 2.0 T 12 days after onset of right flank pain.
(a) Axial T1-weighted MR image (500/30) shows areas of
faint low signal intensity in the right kidney. Diminished
corticomedullary differentiation is also noted. (b) Axial
T2-weighted MR image (2,000/80) shows irregular lowsignal-intensity lesions along the periphery of the right kidney. (c) Postcontrast axial T1-weighted MR image (500/
30) clearly shows nonenhancing infarcted regions and enhancing noninfarcted areas in the right kidney. Note that
the signal intensity of the noninfarcted areas of the right
kidney is higher than that of the uninvolved left kidney.
This finding is also seen in b. (d) Postcontrast coronal
T1-weighted MR image (500/30) shows the same features
as in c and the entire extent of the lesion. (e) Right renal
arteriogram shows occlusion of arterial branches and
nephrographic defects in the peripheral renal cortex. Note
the embolus within the renal artery (white arrow) and the
prominent capsular artery (black arrows). (Reprinted, with
permission, from reference 50.)
capsular blood supply, including collateral circulation from extrarenal arteries. With time, the renal swelling decreases but the low-signal-intensity
rim involving the inner cortex and the columns of
Bertin does not change or slightly thickens (45).
Contrast-enhanced CT demonstrates characteristic findings of renal cortical necrosis, including a
nonenhancing cortical rim that correlates with the
histopathologic findings of the disease (Figs 7c, 8)
(48,49). However, MR imaging is better at demonstrating the extent of the disease because it
does not entail use of iodinated contrast media.
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Figure 10. Renal infarction. MR imaging was performed at 2.0 T 2 days after infarction of the left kidney. (a) Axial
T1-weighted MR image (450/30) shows poor corticomedullary contrast in the left kidney and slightly lower signal
intensity in the anterior portion of the left kidney. (b) Postcontrast axial T1-weighted MR image (450/30) shows a
nonenhancing area of infarction (arrows). Note that the signal intensity of the noninfarcted posterior portion of the
left kidney (arrowheads) is much higher than that of the uninvolved right kidney. (Reprinted, with permission, from
reference 50.)
Arterial Ischemia and Infarction
Infarction of the kidney can result from various
causes, including thromboembolism, renal artery
thrombosis, vasculitis, shock, and trauma.
On both T1- and T2-weighted MR images, the
signal intensity of the infarcted area is usually
lower than that of the noninfarcted area (Fig 9),
although signal intensity may be higher in hemorrhagic infarcts (Fig 10) (50). Corticomedullary
differentiation can be obliterated or less conspicuous in infarcted areas on T1-weighted images
(Fig 9a) (50 –53), and postcontrast T1-weighted
images clearly demonstrate wedge-shaped infarcted areas (Fig 9c, 9d). The extent and distribution of the infarcted areas at MR imaging correlate well with CT and angiographic findings
(Fig 9c–9e) (50). Other findings such as a subcapsular hematoma or fluid collection, mass effect
or a focal area of renal enlargement, and a thickened renal fascia can also be observed on MR images (50 –53).
According to the results of an animal experiment with pathologic correlation (54), the
changes in signal intensity on MR images correlated with the histologic findings and, to an extent, with the age of the infarction. Six hours after
arterial ligation, the kidney showed low signal
intensity on both T1- and T2-weighted images
with the pathologic features of mild interstitial
edema and hemorrhage. From 1 day to 2 weeks
after renal artery ligation, the signal intensity increased progressively with both sequences due to
the initiation of coagulation necrosis and the sequential changes of interstitial hemorrhage in the
infarcted area. Two weeks later, the signal intensity of the infarcted area decreased again with the
pathologic findings of cortical atrophy and organizing fibrosis. Postcontrast T1-weighted images
clearly demonstrated the extent of the lesion (54).
The noninfarcted portion of the involved kidney may have higher signal intensity than the opposite uninvolved kidney on T2-weighted images
and postcontrast T1-weighted images (Fig 10)
(50). This appearance may be attributable to
acute tubular necrosis and interstitial edema at
the margin of the infarct or reperfusion injury following a brief period of ischemia and subsequent
migration of a central occluding embolus from
the main renal artery into peripheral branches
(55). The low signal intensity on both T1- and
T2-weighted images has been explained by lack of
blood perfusion in the early phase and organization of the infarcts in the late phase (56,57). According to the results of an experimental study in
dogs, the main pathologic features of the infarcted
kidney were ischemic tubular damage with prominent interstitial edema in the early stage (up to 7
days) and organization and maturation of the infarct beginning on the 7th day and being well advanced by 17 days after occlusion of the renal arteries (57). MR imaging, especially postcontrast
imaging, can demonstrate the extent of the infarction with an accuracy comparable to that of CT
or angiography without the danger of iodinated
contrast media (51).
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Rejection of a Transplanted Kidney
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Rejection of a transplanted kidney has been reported to show low signal intensity in some cases
(58 – 60). Although loss of corticomedullary differentiation at MR imaging is the most sensitive
indicator in the early evaluation of rejection,
when this entity is combined with diffuse hemorrhagic necrosis or cortical necrosis, low signal intensity may appear in the involved area (58 – 60).
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Conclusions
The kidney is a major organ involved by many
different disease entities with systemic manifestations. Many of them can be diagnosed with intravenous urography, US, and CT. However, because many of these patients have renal dysfunction, iodinated contrast media can aggravate
already impaired renal function. Under these circumstances, MR imaging can be helpful. Some of
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