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4.5 Pericardial Diseases 181
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3 . Weiser NJ et al The postmyocardial infarction syndrome:
the nonspecifi city of the pulmonary manifestations.
Circulation. 1962;25:643–50
4 . Oberholzer K et al Pneumomediastinum and pneumoperi-
cardium due to malignant subcarinal lymphadenopathy:
CT demonstration. Eur Radiol. 1997;7:583–5
5 . Talreja DR et al Constrictive pericarditis in 26 patients with
histologically normal pericardial thickness. Circulation.
2003;108:1852–7
6 . Yousefzadeh DK et al The triad of pneumonitis, pleuritis,
and pericarditis in juvenile rheumatoid arthritis. Pediatr
Radiol. 1979;8:147–50
7 . Spiegel R et al Eosinophilic pericarditis: a rare complica-
tion of idiopathic hypereosinophilic syndrome. Pediatr
Cardiol. 2004;25:690–2
8 . Choi B-R et al Camptodactyly, arthropathy, coax vara, peri-
carditis (CACP) syndrome: a case report. J Korean Med Sci.
2004;19:907–10
9 . Al-Mayouf SM. Familial arthropathy in Saudi Arabian chil-
Fig. 4.5.4 Axial postcontrast cardiac CT with contrast shows
pericardial enhancement ( arrowhead ) with moderate pericardial
effusion in a patient with acute pericarditis
dren: demographic, clinical, and biochemical features.
Semin Arthritis Rheum. 2007;36:256–61
For Further Reading
1 . McIntosh HD. Pericarditis. Dis Mon. 1964;10:1–39
2 . Glockner JF. Imaging of pericardial diseases. Magn Reson
Imaging Clin N Am. 2003;11:149–62
Chapter 5
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Nephrology
CONTENTS
5.1 Hypertension 184
5.2 Polycystic Kidney Disease 196
J. A. Al-Tubaikh: Internal Medicine – An Illustrated Radiological Guide
DOI: 10.1007/978-3-642-03709-2_5, © Springer-Verlag Berlin Heidelberg 2010
183
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5.1
Hypertension
5.1
Hypertension is a disease characterized by an increase
in systolic blood pressure >140 mmHg, and in diastolic
blood pressure >100 mmHg. Hypertension is 90% primary (without a cause), and 10% secondary to an
organic cause. Radiological modalities are mainly used
to detect secondary causes of hypertension.
Secondary causes of hypertension include the
following:
Renovascular diseases : atherosclerosis (adults),
fi bromuscular dysplasia (children), vasculitis (polyarteritis nodosa (PAN) and Takayasu arteritis (TA)),
and renal artery aneurysm.
Adrenal causes : pheochromocytoma, primary hyper-
aldosteronism, and Cushing’s syndrome.
Renal parenchymal diseases : chronic glomerulone-
phritis, diabetic nephropathy, lupus nephritis, polycystic kidney disease, and page kidney.
Aortic diseases : coarctation of the aorta and mid-
aortic syndrome.
Other causes : brain tumors, congenital AVM, carci-
noid tumors, acromegaly, and hypercalcemia.
Sudden renal functions worsening in a hypertensive
patient.
Sudden development or worsening of hypertension
in any age.
Unilateral small kidney.
Renal impairment after treatment with angiotensin-
converting enzymes (ACE) inhibitors.
RAS is commonly diagnosed by color-coded duplex
scanning by two methods: direct and indirect. The
direct method involves measuring the blood velocity
directly within the renal artery (Fig. 5.1.1 ). In contrast,
the indirect method involves measuring the blood
velocity within the segmental and interlobar intra-renal
vessels (Fig. 5.1.2 ). The indirect method is insensitive
for less than 60% RAS.
The resistance index (RI) is the maximal systolic
velocity minus the end diastolic velocity divided by
the maximal velocity. Increase in renal artery RI is
seen in RAS, transplant rejection, acute tubular necrosis, graft infections, and obstructive hydronephrosis.
The RI tends to be high in patients with chronic renal
disease.
Goldblatt kidney is a condition where the kidney
starts to release rennin to overcome RAS, leading to
renovascular hypertension. Page kidney , on the other
hand, is a condition where the kidney is compressed
from an adjacent pathology that causes cortical ischemia. The kidney releases rennin to overcome the ischemia, leading to renovascular hypertension.
Renal Artery Stenosis
Renal artery stenosis (RAS) constitutes 1–5% of
patients with hypertension. Atherosclerosis is the commonest cause of renovascular hypertension in adults,
while renal artery fi bromuscular dysplasia is the most
common cause of renovascular hypertension in children. Atherosclerosis RAS often affects the proximal
part of the artery, while fi bromuscular dysplasia often
involves the middle and the distal part in a form of
small stenotic and aneurysmal dilatation, giving the
so-called “beaded appearance” on angiography.
RAS is suspected as a cause of hypertension in the
following situations:
Hypertension in a patient <30 years of age, or a
patient >50 years.
Hypertension that is resistant to three antihyperten-
sive regimens.
The Normal Renal Artery Waveform Parameters
The normal renal artery waveform shows low resis-
tance, continuous profi le through the cardiac cycle, with
an RI <0.7. Also, the normal main renal artery waveform has an early systolic peak (ESP) (Fig. 5.1.3 ).
The renal-aortic ration ( RAR ) is defi ned as the maxi-
mum peak systolic velocity (PSV) of the renal artery
divided by the maximum PSV of the aorta at the
level of the superior mesenteric artery (SMA). A
high false RAR can be seen in cases of abdominal
aortic aneurysm, and aortic PSV <40 cm/s, or aortic
PSV >125 cm/s. Also, RAR should not be used in
the assessment of renal artery aneurysm for young
patients or patients with renal artery stents.
The normal interlobar and segmental arteries display
an ESP at the beginning of the systole. The ESP is
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Fig. 5.1.1. Color Doppler
sonogram of the aorta shows
a normal anatomy of the renal
arteries (Banana peel view) in
gray-mode in ( a ) and Duplex
colored mode in ( b ) taken
while the patient is in the
lateral decubitus position. The
right renal artery is clearly
detected in ( b ) ( yellow
arrowhead ), and the left renal
artery is also detected well in
this position ( blue arrowhead )
Fig. 5.1.2. Color Doppler
sonogram of the left kidney
demonstrates its vascular
anatomy in ( b ) and arterial
waveform detection in ( a ) to
assess the arterial vascular
supply as an indirect method
for detecting RAS
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Fig. 5.1.3. Color Doppler
sonogram of the renal arteries
demonstrates normal arterial
waveform of the right renal
artery ( a ) and the left renal
artery ( b )
5.1
absent when the arterial stenosis is >60%. The
Doppler angle should be <30°; otherwise the peak
will not be demonstrated.
The systolic acceleration time ( SAT ) is defi ned as the
time measured from the start of the systolic upstroke
to the fi rst ESP. Normally it is <0.07.
Signs of Direct RAS on Doppler Sonography
High renal parenchymal echogenicity that may reach or
exceed the liver echogenicity (signs of renal parenchymal
damage). A kidney disease can cause renal artery resistant
waveform, which may be mistaken with RAS.
Normal RAR (<3.5) and the normal renal PSV (<180 cm/s).
Sixty percent RAS shows RAR <3.5, with PSV between 180
and 200 cm/s. There is no poststenotic turbulence (mosaic
pattern/ aliasing artifact) with RAS <60%. A 60–99% RAS
shows RAR >3.5, PSV >200 cm/s, and poststenotic
turbulence.
Signs on Indirect RAS on Doppler Sonography
Absence of the ESP.
An accelerated time peak >100 ms is consistent with >60%
stenosis.
Tadus parvus waveform : this waveform consists of slow,
damped systolic acceleration (tardus) and rounding and
fl attening of the systolic peak (parvus).
More than (−5) diff erence between the two kidneys RI.
Kidney size <9 cm, or the diff erence in size between the two
kidneys >2 cm in diameter (normal kidney size = 9–12 cm in
diameter).
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Signs on CT
Arterial cut-off sign : the course of the renal artery is seen
interrupted on contrast- enhanced images. It is a sign of renal
artery obstruction (Fig. 5.1.4 ).
Rim sign of vascular compromise
: the kidney fails to enhance on
contrast-enhanced images, with a thin rim of subcapsular
enhancement seen paralleling the renal margin (Fig. 5.1.4 ).
This sign is caused by renal medullary arterial perfusion
interruption in cases of renal artery obstruction, with preserved
perfusion of the renal cortex by the capsular perforating
vessels. This sign can be seen in cases of renal vein thrombosis,
renal arterial occlusion, and acute tubular necrosis.
: this sign is seen as hypodense renal cortex
Reverse rim sign
against a contrast-enhanced background of intact meullary
arterial perfusion (Fig. 5.1.4 ). This sign is seen in cases of
compromised renal arterial perfusion in cases of cortical
necrosis.
Fig. 5.1.5. MRA image shows >50% stenosis of the left renal
artery ( arrowhead ) in a patient with peripheral vascular disease
Fig. 5.1.4. Axial postcontrast-enhanced CT illustration shows
the arterial cut-off sign ( solid arrowhead ), rim sign of vascular
compromise ( open arrowhead ), and reverse rim sign ( arrow )
Signs on MRA
Magnetic resonance angiography (MRA) demonstrates the
aortic vessels clearly and it is mostly used after detection of
RAS on Doppler sonography for surgical planning (Fig. 5.1.5 ).
Coarctation of the Aorta
Coarctation of the aorta is a condition characterized by
aortic lumen narrowing, most commonly located below
the origin of the left subclavian artery (the aortic isthmus near the ligamentum arteriosum), causing hypertension below the level of the narrowing.
Patients with aortic coarctation often present with
severe hypertension that does not respond to antihypertensive medication and chest pain that radiates to
the back. Patients with aortic coarctation carry the risk
of aortic dissection, which is characterized by aortic
wall intimal tear and leaking of the blood in between
the aortic wall layers.
When it is chronic, aortic coarctation causes dilatation of the internal mammary and intercostals arteries.
Chronic high-pressure pulsation of the intercostals
arteries over the inferior aspect of the ribs may result
in rib notching. Coarctation of the aorta can be seen in
up to 30% in patients with bicuspid aortic valve.
Pseudo-coarctation of the aorta is a relatively rare
condition characterized by kinking of the aorta at its
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isthmus near the ligamentum arteriosum without lumen
narrowing. Pseudocoarctation resembles true coarctation; differentiation is possible by looking for changes
of the collateral circulation, where there will be no
enlarged peripheral vessels, signs of pressure gradients,
5.1
or rib notching. The condition is symptomless, and can
be associated with congenital bicuspid aortic valve.
Signs on Chest Radiograph
In chronic cases of aortic coarctation, the ribs show irregular
lower border representing rib notching (Fig. 5.1.6 ). This
condition can be also seen in other conditions aff ecting the
intercostals neurovascular bundle like superior vena cava
obstruction syndrome and neurofi bromatosis of the
intercostals nerves.
The aortic arch is often bulging with dilatation of the aortic
knuckle (Fig. 5.1.7 ).
Pseudocoarctation of the aorta is seen as elongated aortic
knuckle appearing like a posterior mediastinal mass.
Fig. 5.1.7. Posteroanterior plain chest radiograph in a patient with
coarctation of the aorta shows bulging of the aortic knuckle
Signs on CT and MRI
Aortic coarctation classically is seen in sagittal reformatted
images as a narrowing of the aortic lumen located at the area
of the aortic isthmus, giving the classic “inverted shape of 3”
(Fig. 5.1.8 ).
Aortic dissection is seen as hypodense layer found within the
aortic lumen on postcontrast-enhanced images representing
the false lumen (Fig. 5.1.9 ). Stanford type A dissection involves
dissection of the ascending aorta and the arch up to the origin
of the left subclavian artery. Stanford type B dissection
involves dissection of the descending aorta below the origin
of the subclavian artery. Type A is managed surgically, while
type B is managed medically, providing evidence of
end-organ ischemia not being present.
Aortic pseudocoarctation is seen on axial CT images as higher
than normal located arch, with a well-defi ned enhancing
vascular mass located near the aortic arch, representing the
kinked portion of the arch.
Fig. 5.1.6. Plain chest radiograph shows rib notching in a patient
with severe aortic coarctation since 12 years ( arrowheads )
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Polyarteritis Nodosa
Polyarteritis nodosa is a rare disease characterized by
aneurismal, nodular lesions that affect the mediumsized and small-sized arteries due to fi brinoid necrotizing vasculitis.
Vasculitides are a diverse group of diseases characterized by infl ammation and necrosis of all three coats
of the vessels (intima, media, and adventitia). They are
divided into large-vessels vasculitis (e.g., Takayasu
and giant cell arteritis), medium-sized vessels vasculitis (e.g., polyarteritis nodosa and Kawasaki disease),
and small-sized vessels (e.g., Wegener’s granulomatosis and Henoch-Schönlein purpura).
Polyarteritis nodosa commonly causes multiple
arterial aneurismal wall formation, plus fragmentation
and degeneration of the adventitia layer. Necrosis starts
in the media layer, and spreads to involve the entire
width of the vascular wall. This infl ammation and
necrosis is associated with eosinophilic infi ltration,
fi brin deposition, and destruction of the elastic tissue
and the intima layer. Vascular thrombosis or an aneurysm, mainly at the vessels bifurcation or the hilar
region of viscera, may occur. Later, a granuloma is
formed at the area of previous infl ammation with fi broblasts proliferation. A healed stage is characterized by
vascular recanalization, and formation of a nonvascu-
Fig. 5.1.8. Sagittal MRA of a patient with coarctation of the
aorta shows the inverted shape of 3, which is characteristic of
this condition ( arrowhead )
Fig. 5.1.9. Axial CT-angiography shows the classical intimal
fl ap in a patient with aortic dissection Stanford type A
larized fi brous mass that completely replaces a section
of the vessel wall. The disease rapidly progresses once
started, and death may result from strokes or myocardial infarctions within 2–3 months after onset.
Any organ can be affected by PAN, including the central and peripheral nervous system. The kidney is the
most commonly involved (80–90%), followed by the
gastrointestinal (GI) tract (50–70%). Clinically, patients
present with vague signs and symptoms like fever, myalgia, headache, and malaise. Renal artery involvement,
especially at the renal hilum, often results in rapidly progressing hypertension. Involvement of the GI tract may
present with lower GI bleeding, abdominal pain, and
vomiting (6% of cases). Peripheral nervous system
involvement compromises the nervous tissue blood supply causing polyneuropathy. Other lesions involve pericarditis, myocardial infarction, and purpuric skin rash.
Up to 30% of patients test positive to hepatitis B surface
antigens, and up to 50% of patients have arthralgias.
Laboratory investigations usually show leucocytosis with eosinophilia (4%), anemia, uremia, and high
erythrocyte sedimentation rate.
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5.1
Signs on Angiography or MRA
Polyarteritis nodosa is suggested by detection of multiple
aneurysms up to 1 cm in diameter within the renal, mesenteric,
hepatic, or central venous vasculature. This fi nding is not
pathognomonic since it can be seen in patients with necrotizing
angiitis associated with drug-abuse. The history and the high
suspicion of PAV with this angiographic picture help to
diff erentiate the two entities.
Signs on CT
The bowel walls are thickened and show white-attenuated
target sign after contrast injection.
CT-angiography shows multiple aortic aneurysms in the
branches of the SMA or the celiac trunk.
Spotted nephrogram : small vessels occlusion in cases of PAN
may cause patchy perfusion of the kidney on IVU or
contrast-enhanced CT due to multiple infarctions (Fig. 5.1.10 ).
This sign can be also seen in scleroderma and hypertensive
nephrocalcinosis.
limb ischemia. The disease affects mainly the aorta
and its major branches.
TA affects mainly young females between 20 and 30
years of age, who present with nonspecifi c systemic
infl ammatory symptoms like fever, night sweat, weight
loss, myalgia, and arthralgia. TA has two main phases
with different clinical presentations, an early and a late
phase. The early phase is characterized by nonspecifi c
infl ammation in the blood vessels walls affecting the
media and the adventitia layers. These nonspecifi c
infl ammatory changes are responsible for the nonspecifi c, systemic infl ammatory symptoms. In contrast, the
late phase is characterized by arterial symptoms with no
systemic symptoms. The absence of the systemic symptoms in the late phase is attributed to the development of
systemic collaterals; however, this is not seen in all
patients. In the late phase, the coronary arteries might
be affected. Hypertension, arterial stenosis, aneurysms,
and dissection all can be seen in late phase of TA.
Criteria for TA diagnosis (TA Diagnosis Requires
At Least Three Criteria)
Takayasu Arteritis
Takayasu arteritis is a rare, granulomatous disease
characterized by infl ammation of the large vessel
walls, leading to progressive stenosis, aneurysms, or
Fig. 5.1.10. Axial CT illustration demonstrates the spotted nephrogram that may be seen in patients with polyarteritis nodosa
Age of presentation <40 years.
Limbs caludication.
Decrease one or both brachial arteries pulse.
Blood pressure difference of the extremities >10 mmHg.
Bruit heard over the aorta or the subclavian arteries.
Angiographic abnormalities include arterial occlu-
sion, stenosis or aneurysms of the aorta or its main
branches. Commonly, these abnormalities are observed
bilaterally.
Signs on CT and CT-Angiography
In the acute phase, there is thickening of the great vessels
wall without signs of calcifi cation due to infl ammation and
intramural hematomas (especially the aorta) (Fig. 5.1.11 ).
The thickened vascular wall may show enhancement in early
contrast-phase due to infl ammatory hyperemia.
Aneurysmal dilatation of the aortic root or its major branches
is mainly observed in late chronic phase of the disease.
Signs of dissection, stenosis or occlusion of the major vessels
may be seen (Fig. 5.1.12 ).
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MAS classically starts from the infra-renal part of
the aorta and progresses proximally to involve the
renal arteries (80%), SMA, and the celiac artery (25%).
MAS mainly affects children and young adults who
typically present with renovascular hypertension due
to bilateral RAS. If untreated, the disease is fatal by the
age of 30, with many patients experiencing intracranial
bleeding due to malignant hypertension. The inferior
mesenteric artery (IMA) and the common iliac arteries
are almost never involved.
How can you differentiate between MAS and TA?
Takayasu arteritis often present with systemic symp-
toms of fever, malaise, and weight loss. These fea-
Fig. 5.1.11. Axial CT-angiography in a 50-year-old female patient
presented with nonspecifi c systemic infl ammatory symptoms
with absent right arm pulsation and limb claudication. Patient
was suspected to have Takayasu arteritis by the attending physician. CTA confi rmed the acute thickening of the aortic wall
( arrowheads ), with occlusion of the right subclavian artery and
multiple aneurysms affecting the carotid arteries (not shown)
tures are not part of MAS.
MAS affects mainly children and young adults,
while Takayasu arteritis mainly affects females
between 20 and 30 years of age.
MAS exclusively affects the mid-abdominal aorta,
while Takayasu arteritis involves any vessels and can
even affect the pulmonary artery, causing pulmonary
hypertension.
Fig. 5.1.12. Aortic-renal angiography in a patient with chronic
Takayasu arteritis shows multiple small stenoses and dilatations
affecting the right renal artery and the abdominal aorta in a
milder degree
Midaortic Syndrome
Midaortic syndrome (MAS) is a nonspecifi c arteritis
that affects the mid-portion of the abdominal aorta and
its main branches.
Signs on Doppler Sonographs
Stenosis of the mid-abdominal aorta.
Renal artery stenosis is often seen unilaterally or bilaterally.
Signs on CT-Angiography
The aorta shows stenosis typically from the infrarenal portion,
and extends proximally to involve the renal arteries, IMA, or
the celiac.
The IMA and the common iliac vessels are spared.
Preeclampsia
Preeclampsia is a pregnancy-related condition characterized by hypertension, lower leg edema, and protienuria. In contrast, eclampsia is a life-threatening
condition characterized by the same symptoms as
preeclampsia plus tonic-clonic seizures.
Hypertensive disorders occur in about 3–10% of all
pregnancies, and the incidence of preeclampsia ranges
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