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Chapter 3 · Endocrinology andMetabolism
Signs on Plain Radiographs
Gynecomastia is detected as unilateral or bilateral breast
shadow enlargement (. Fig. 3.10.4 ).
3
. Fig. 3.10.4 A plain chest radiograph of a patient with
gynecomastia demonstrates unilateral enlarged breast shadow
. Fig. 3.10.5 Axial T1W nonenhanced MR illustration
demonstrates left-sided multilobulated ovarian mass with internal
small cystic lesions representing ovarian Sertoli cell tumor
Intersex Disorders
Signs on US
5 Leydig cell tumors are seen as hypoechoic lesions
within the testes with peripheral vascularity on
color Doppler sonography. Larger tumors show
cystic changes and mixed echo-texture. Large-cell
calcifying Leydig cell tumors are detected as
multiple areas of high echogenicity with acoustic
shadowing representing calcification.
5 Testicular Sertoli cell tumors are seen usually as
bilateral hypoechoic lesions with areas of dense
echogenic foci due to calcified scars (burned-out
appearance) or as multicystic lesion arranged in a
“spoke wheel” configuration.
Signs on MRI
5 Testicular Sertoli cell tumors show low T1 and high
T2 signal intensity with marked contrast
enhancement after contrast injection. History and
elevated androgen or estrogen serum levels are
important supportive tools for diagnosis.
5 Ovarian Sertoli cell tumor is detected as unilateral,
multilobulated mass with or without internal cysts.
The mass can show low T2 signal depending on
the extents of fibrous stroma. After contrast
injection, the cells show intense heterogeneous
contrast enhancement (. Fig. 3.10.5 ) .
Intersex disorders are a group of diseases characterized by
ambiguous genitalia and abnormalities in sexual di erentiation. Ambiguous genitalia are de ned as external genitalia
that do not have a typical male or female anatomic appearance. A person’s phenotypic sex results from the di erentiation
of the Müllerian ducts and external genitalia under the in uence of hormones and transcription factors.
ere are four main categories of intersex disorders:
female pseudohermaphroditism, gonadal dysgenesis, true
hermaphroditism, and male pseudohermaphroditism.
Imaging plays a role in detecting abnormalities in the internal
pelvic sex organs and early detection of malignant masses
formed within these organs. ere is an increased prevalence
of stromal and gonadal tumors in patients with intersex
disorders. Image analysis included evaluation of the presence
or absence of the uterus, ovaries, testes, penis, and clitoris.
Female Pseudohermaphroditism
Female pseudohermaphroditism is a female genetically
(46, XX) with two ovaries for gonads, but their external
genitalia show a variable degree of virilization due to
exposure to excess androgens in utero. Virilization refers
to male sexual characteristics due to androgen exposure.
Female pseudohermaphroditism most commonly arises
due to congenital adrenal hyperplasia ( CAH ). In CAH, there
are enzymatic defects in cortisol production pathway at certain key positions. ese enzymatic defects cause excessive
accumulation of the intermediate steroid compounds that
3.10 · Sex Hormone Abnormalities
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are produced before the metabolic block. Some of these
intermediate steroids are converted into androgenically
active substances. is excess androgen exposure causes
virilization of the external genitalia, which is manifested
commonly as enlarged clitoris (clitoromegaly).
Signs on US
CAH is seen as enlarged adrenals located above the
kidneys with a “cerebriform pattern” (the adrenal glands
have multiple coils that look like cerebral gyri). The
adrenal gland limbs are commonly over 20mm long,
4mm wide, and with normal corticomedullary
di erentiation.
Signs on MRI
5 MRI demonstrates masculinized external genitalia
with normal ovaries, fallopian tubes, uterus, and
vagina. The clitoris mimics a small penis due to
prominent corpora cavernosa and corpus
spongiosum (. Fig. 3.10.6 ).
5 The vagina and the uterus may be filled with urine
due to urogenital sinus formation.
. Fig. 3.10.6 Sagittal T1W pelvic MR illustration demonstrates
enlarged clitoris with prominent corpora cavernosa and
corpus spongiosum ( black arrowhead ) with normal vagina and
uterus ( white arrows ) in a patient with female
pseudohermaphroditism
167
Male Pseudohermaphroditism
In male pseudohermaphroditism, patients are genetically
male (46, XY) with two testes for gonads, but their
external genitalia show a variable degree of feminization
due to a defect in the testes or testosterone metabolism.
e phenotype of the male pseudohermaphroditism
ranges from completely female external genitalia to a mild
male phenotype with hypospadia or cryptorchidism.
Cryptorchidism is a condition characterized by both abnor-
mal testicular development and failure of the intra-abdominal testes to descend into the scrotum. e testes may be
located at any point along the normal descent route. is
condition can be seen in up to 30 % in premature infants and
up to 8.8 % in full-term infants.
Male pseudohermaphroditism can be classi ed into eight
groups according to the etiology:
5 Leydig cell failure : Leydig cells are testicular cells that
secrete testosterone in males. Failure of testosterone
secretion results in male pseudohermaphroditism.
5 Testosterone synthesis defects : any cause of testosterone
synthesis results in male pseudohermaphroditism.
5 Androgen insensitivity syndrome (AIS) ( Morris
syndrome ): this syndrome, also known as testicular
feminization syndrome , arises due to insensitivity of the
body cells to testosterone due to mutation of the
steroid-binging receptors. Children with AIS exhibit a
female external genitalia, although the karyotype is (46,
XY), and testes are located internally. Most patients with
AIS are not diagnosed until puberty, when they are
investigated for amenorrhea.
5 5α-Reductase de ciency is an autosomal recessive
condition characterized by a defect in conversion of
testosterone to the active form dihydrotestosterone
through the enzyme 5α-reductase.
5 Persistent Müllerian duct syndrome ( PMDS ): as
mentioned before, Sertoli cells are supporting cells and
phagocytes. In the embryo, Sertoli cells secrete
anti-Müllerian inhibitory substances that cause apoptosis
and regression of the Müllerian ducts, facilitating the
male phenotype development. Failure of Sertoli cells to
secrete the Müllerian inhibitory substances results in
male pseudohermaphroditism.
5 Testicular dysgenesis : abnormal formation of the testes
can result in male pseudohermaphroditism.
5 Congenital anorchia ( vanishing testes syndrome ) is a
disease where the testes are absent. Loss of the testes
before 8 weeks’ gestation results in a male (46, XY) with
female external and internal genitalia. A loss of testes
function a er the critical male di erentiation period at
12–14 weeks’ gestation results in a normal male
phenotype externally with anorchia internally.
5 Exogenous source : due to insult to the male development
mechanism in utero, o en due to maternal ingestion of
progesterone or estrogen or various environmental hazards.
3
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Chapter 3 · Endocrinology andMetabolism
D i erential Diagnoses andRelated
Diseases
5 PAGOD (Mecham) syndrome is an extremely rare disease
characterized by pulmonary artery hypoplasia,
3
agonadism, omphalocele/diaphragm defect, and
dextrocardia. Most infants die shortly a er birth due to
cardiopulmonary problems.
5 Denys–Drash syndrome ( DDS ) is a disease characterized
by male pseudohermaphroditism, progressive
glomerulopathy, and urinary tract tumors (e.g., Wilms’
tumor). Nephropathy starts in infancy as a di use
mesangial sclerosis and rapidly progresses to end-stage
renal failure by the age of 3 years. DDS have overlap
manifestations with Mecham syndrome, which is
characterized by congenital diaphragmatic hernia, double
vagina, sex reversal, and cardiac malformations. Unlike
DDS, those with Mecham syndrome do not develop
Wilms’ tumor.
5 Fraser syndrome is a disease characterized by male
pseudohermaphroditism, progressive glomerulopathy,
and urinary tract tumors (e.g., Wilms’ tumor). Unlike
DDS, nephropathy is a steroid-resistant focal segmental
sclerosis, and it starts in childhood and progresses to
end-stage renal failure by the second or third decade of
life. Both Fraser and DDS may present with congenital
diaphragmatic hernias.
5 Aarskog (facial–digital–genital) syndrome is a disease
characterized by characteristic short status and facial
features (e.g., hypertelorism), digital abnormalities (e.g.,
short ngers), and genital abnormalities (e.g.,
cryptorchidism). Radiographic ndings of Aarskog
syndrome show maxillary hypoplasia, hypoplasia of
terminal phalanges of ngers, spina bi da occulta, and
hypoplastic middle phalanges of the toes. Children with
Aarskog syndrome may show features of growth
hormone de ciency.
5 LEOPARD syndrome is a disease characterized by
lentigines (pathognomonic), electrocardiographic (ECG)
conduction defects, ocular hypertelorism, pulmonary
stenosis, abnormal genitalia, retardation of growth, and
sensorineural deafness. To establish LEOPARD
syndrome diagnosis, lentigines and two of the other
characteristic features need to be ful lled. e disease has
an autosomal dominant mode of inheritance.
Signs on CT and MRI
5 Both testes are present either in the scrotum or in the
inguinal canal (undescended testes). The external
genitalia are incompletely masculinized or frankly
ambiguous. Prostatic tissue appears to be present.
5 AIS : patients with AIS may show cystic lesions
within the pelvis representing residual parts of the
Müllerian system. It is important to screen patients
with male pseudohermaphroditism radiologically
because of the high risk of malignant
transformation of the nonfunctioning Müllerian
system residuals. Bilateral gonadectomy is
recommended in patients with AIS because of the
high incidence of seminomas.
5 PMDS : patients with PMDS are males with uterus
and fallopian tubes inside their pelvis. Two forms
are present, the male and the female forms. The
male form, also called hernia uteri inguinale , is
characterized by a male with one testis descended
in the scrotum and the other testis located at the
contralateral ovary position in the pelvis. In the
female form, the phenotype is of a female with a
hypoplastic, blind-ended uterus located behind
the bladder. The testes are bilaterally located in the
“ovarian” position (not within the scrotum)
(. Fig. 3.10.7 ) .
. Fig. 3.10.7 Axial pelvic CT illustration demonstrates the
female form of persistent Müllerian duct syndrome (PMDS). The
uterus is detected behind the bladder ( arrow ), and the testes
are located at the position of the ovaries bilaterally
( arrowheads )
Signs on US
Cryptorchidism can be detected by US as an isoechoic or
hypoechoic mass relative to the normal testes located in
the inguinal canal (70 % of cases) or the prescrotal region
just beyond the external inguinal ring (20 %).
True Hermaphroditism
In true hermaphroditism, patients have both ovaries and
testes for gonads, often due to chromosome mosaicism
( chimerism ).
There are three types of true hermaphroditism:
5 Lateral true hermaphroditism : patients have a testis
on one side and an ovary on the other side in the
pelvis.
3.10 · Sex Hormone Abnormalities
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169
3
5 Unilateral true hermaphroditism : patients have both
a testis and an ovary on one side and a testis or an
ovary on the other side of the pelvis.
5 Bilateral true hermaphroditism : patients have both
a testis and an ovary on both sides of the pelvis.
Patients with true hermaphroditism also show ambiguous
genitalia, with hypospadia, cryptorchidism, and incomplete
fusion of the labioscrotal folds.
Signs on MRI
5 The external genitalia are ambiguous.
5 There are both testes and ovaries found in the
pelvis according to the type (lateral, unilateral, or
bilateral).
5 Hypoplastic uterus is found in almost all cases.
Gonadal Dysgenesis
Patients with gonadal dysgenesis are male
pseudohermaphroditism with Müllerian duct structures.
Gonadal dysgenesis disorders are a spectrum of
anomalies that include pure gonadal dysgenesis, partial
gonadal dysgenesis, and mixed gonadal dysgenesis. In
pure gonadal dysgenesis, patients have bilateral streak
gonads (dysfunctional gonads without germ cells). In
mixed and partial gonadal dysgenesis, there is one testis
on one side and a streak gonad on the other side.
Gonadal dysgenesis is characterized by defect in the sex
determination region on chromosome Y (SRY). e infant
initially starts as a male karyotype (46, XY), but due to the
failure in the SRY, the testes are not developed and the female
development takes place (sex reversal), despite the presence
of the Y chromosome. e patient is a female with XY karyotype and Müllerian derivatives including uterus, fallopian
tubes, and cervix. Turner syndrome (45, XO) is an example of
gonadal dysgenesis disorder.
Swyer syndrome is an uncommon form of pure gonadal
dysgenesis. e male child with Swyer syndrome looks
female externally, but the karyotype is (46, XY) with a nonfunctioning Y chromosome. Patients with Swyer syndrome
may have multiple pterygium syndrome , which is character-
ized by multiple body contractures since birth with webbing
of the neck, elbows, knees, and intracrural areas.
Streak gonads should be removed surgically because the
risk of malignant transformation within the rst two decades
of life can reach up to 30 % of cases.
Signs on MRI
The patient shows both testes and Müllerian duct
derivatives (e.g., uterus) (. Fig. 3.10.8 ).
Streak gonads are di cult to detect and usually seen
as low signal intensity stripes on T2W images. High signal
intensity of streak gonads on T2W images could
represent a sign of malignant transformation.
. Fig. 3.10.8 Sagittal T1W pelvic MR illustration
demonstrates ndings in a patient with gonadal dysgenesis.
There is vagina with absent uterus representing Müllerian duct
derivatives ( white arrow ), in the presence of the penis ( black
arrowhead )
Further Reading
Angle B etal. XY gonadal dysgenesis associated with a mul-
tiple pterygium syndrome phenotype. Am J Med Genet.
1997;68:7–11.
Aso C et al. Gray-scale and color Doppler sonography of
scrotal disorders in children: an update. Radiographics.
2005;25:1197–214.
Browne LP etal. Van Wyk and Grumbach syndrome revis-
ited: imaging and clinical ndings in pre- and postpubertal girls. Pediatr Radiol. 2008;38:538–42.
Chavhan GB etal. Imaging of ambiguous genitalia: classi ca-
tion and diagnostic approach. Radiographics. 2008;28:
1891–904.
Chen H-Y etal. Pure XY gonadal dysgenesis and agenesis in
monozygotic twins. Fertil Steril. 2006;85:1059.e9–11.
170
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Chapter 3 · Endocrinology andMetabolism
Cho HY etal. Hydrothorax in a patient with Denys-Drash
syndrome associated with diaphragmatic defect. Pediatr
Nephrol. 2006;21:1909–12.
Choi HK etal. MR imaging of intersexuality. Radiographics.
1998;18:83–96.
3
Christensen JD et al. e undescended testis. Semin
Ultrasound CT MR. 2007;28:307–16.
Elon Gale M.Hermaphroditism demonstrated by computed
tomography. AJR Am J Roentgenol. 1983;141:99–100.
Erdem CZ et al. Polycystic ovary syndrome: dynamic
contrast- enhanced ovary MR imaging. Eur J Radiol.
2004;51:48–53.
Franceschi R etal. Prevalence of polycystic ovary syndrome
in young women who had idiopathic central precocious
puberty. Fertil Steril. 2009. doi:10.1016/j.fertnstert.2008.11.016.
Hedlund GL etal. Disorders of puberty: a practical imaging
approach. Semin Ultrasound CT MR. 1994;15:49–77.
Hernanz-Schulman M etal. Sonographic ndings in infants
with congenital adrenal hyperplasia. Pediatr Radiol.
2002;32:130–7.
Hyun G etal. A practical approach to intersex in the newborn
period. Urol Clin North Am. 2004;31:435–43.
Jagadhish LCTK.Van Wyk and Grumbach syndrome (a syn-
drome of incomplete isosexual precocity and juvenile hypothyroidism). Armed Forces Med J India. 2002;58:343–5.
Johnsen DE etal. MR imaging of the sellar and juxtasellar
regions. Radiographics. 1991;11:727–58.
Jung SE etal. CT and MRI ndings of sex-cord stromal tumor
of the ovary. AJR Am J Roentgenol. 2005;185:207–15.
Karabulut N etal. Stromal tumor of the sex cord in a woman
with testicular feminization syndrome: imaging features.
AJR Am J Roentgenol. 2002;178:1496–8.
Kim JB etal. A case of PAGOD syndrome with hypoplastic
le heart syndrome. Int J Cardiol. 2007;114:270–1.
Kodama M et al. Aarskog syndrome with isolated growth
hormone de ciency. Eur J Pediatr. 1981;135:273–6.
Narlawar RS etal. Persistent mullerian duct syndrome with
teratoma in an ectopic testis: imaging features. Eur Radiol.
2001;11:955–8.
Sharafuddin MJA etal. MR imaging diagnosis of central pre-
cocious puberty: importance of changes in the shape and
size of the pituitary gland. AJR Am J Roentgenol.
1994;162:1167–73.
Wang Y-C etal. Maternal and female fetal virilization caused
by pregnancy luteoma. Fertil Steril. 2005;84:509.e15–7.
Woodward PJ etal. Tumors and tumorlike lesions of the tes-
tes: radiologic-pathologic correlation. Radiographics.
2002;22:189–216.
Wu H-C etal. Persistent Müllerian duct syndrome with sem-
inoma: CT ndings. AJR Am J Roentgenol. 2000;174:
102–4.
Yagubyan M et al. LEOPARD syndrome: a new polyaneu-
rysm association and an update on the molecular genetics
of the disease. J Vasc Surg. 2004;39:897–900.
Yanai Y etal. Androgen insensitivity syndrome with serous
gonadal cyst. Fertil Steril. 2008;90:2018.e9–11.
3.11 Sheehan Syndrome (Postpartum
Hypopituitarism)
Sheehan’s syndrome (SS), previously known as Simmonds’
disease ( pituitary cachexia ), is a rare condition characterized
by infarction and necrosis of the anterior pituitary gland
(adenohypophysis) due to postdelivery hemorrhage.
e normal pituitary gland shows physiological changes
in size according to age: infants and children 6mm in diameter, men and postmenopausal women 8mm in diameter,
and childbearing women 10mm in diameter, and women in
late pregnancy and puerperium may reach up to 12mm in
diameter. SS is attributed to an increased size of the pituitary
gland during pregnancy, which may compress over the superior hypophyseal artery and thereby cause a mild ischemia. If
sudden change in the arterial pressure occurs during or a er
delivery due to severe hemorrhage or hypotension, arterial
spasm in the small vessels and pituitary infarction (apoplexy)
may occur. However, SS may rarely occur without postpartum bleeding.
Patients with SS are characterized by postpartum delivery
hemorrhage, hypovolemia, and disseminated intravascular
coagulation (DIC), usually due to retained placenta products.
A relatively small sella size was suggested as a risk factor for
the development of SS.
SS patients o en present a er a period of 6 months to
24 years a er a hemorrhagic delivery with di erent clinical manifestation according to the progression of the condition. Acute manifestations of SS include pituitary
apoplexy. Patients present with sudden headache (95 %)
due to stretching and irritation of the dura matter in the
wall of the sella, because it is supplied by the meningeal
branches of the trigeminal nerve. Other features include
ocular paresis due to abducens and oculomotor nerve
compression within the cavernous sinus and vomiting
(69 %) due to increased intracranial pressure or meningeal
irritation.
Chronic or delayed manifestations of SS are all related to
adenohypophysis dysfunction with a wide spectrum of
symptoms. e most common manifestation is postpartum
lactation failure (agalactia). Growth hormone is one of the
earliest hormones lost in SS, and it may result in constitutional symptoms like weakness, malaise, and fatigue.
Amenorrhea and postpartum menstruation failure are other
common complaints in SS.Residual pituitary function may
be su cient to conceive in some patients, which means that
the presence of pregnancy is not against SS in patients who
su ered from pituitary apoplexy in the past. Secondary hypothyroidism and adrenocortical insu ciency may occur.
Interestingly, women with SS may show premature pale aging
face with ne wrinkling around the mouth and the eyes due
to long-term growth hormone and estrogen de ciency that
result in skin aging.
Apart from the hormonal abnormalities, laboratory ndings in SS include normocytic normochromic anemia, hyponatremia, and hypoglycemia.
3.11 · Sheehan Syndrome (Postpartum Hypopituitarism)
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171
3
Signs on CT
In pituitary apoplexy, CT will show an enlarged pituitary
gland with hyperdense areas as a sign of hemorrhage
and hypodense areas as a sign of necrosis (. Fig. 3.11.1 ).
Contrast injection shows hyperdense rim enhancement
with hypodense center due to infarction.
. Fig. 3.11.2 Sagittal T1W postcontrast MR illustration of the
sella demonstrates a thick rim enhancement in a patient with SS
due to pituitary apoplexy
. Fig. 3.11.1 Axial unenhanced brain CT shows hyperdense
area in the region of the sella as an area of hemorrhagic
infarction in a patient with Sheehan’s syndrome (SS)
( arrowhead )
Signs on MRI
5 The normal postpartum pituitary is hyperintense
on T1W images and can measure up to 12mm in
diameter. In the acute stage of SS, the pituitary is
enlarged (>12mm) and bulging under the optic
chiasma. Areas of hypointensity on T1W and
hyperintensity on T2W images representing
infarction may be seen. After gadolinium injection,
the gland shows thick homogeneous peripheral
ring enhancement with hypointense center due to
infarction and hyperemia (. Fig. 3.11.2 ).
5 In the chronic stage of SS, the MR scan usually
shows empty sella.
Further Reading
Dejager S etal. Sheehan’s syndrome: di erential diagnosis in
the acute stage. J Intern Med. 1998;244:261–6.
Gokalp D etal. Sheehan’s syndrome as a rare cause of anae-
mia secondary to hypopituitarism. Ann Hematol.
2009;88:405–10.
K e l e ştimur F.Sheehan’s syndrome. Pituitary. 2003;6:181–8.
Vaphiades MS et al. Sheehan syndrome: a splinter of the
mind. Surv Ophthalmol. 2003;48:230–3.
Weiner HA. Simmond’s disease. Yale J Biol Med. 1937;10:
31–9.
Nephrology
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4.1 Hypertension – 174
Renal Artery Stenosis – 174
Coarctation oftheAorta – 178
Polyarteritis Nodosa – 179
Takayasu Arteritis – 180
Midaortic Syndrome – 181
Preeclampsia – 181
Reversible Posterior Leukoencephalopathy
Syndrome (Hypertensive Encephalopathy) – 182
Nephroptosis (Floating Kidney) – 183
Riley–Day Syndrome (Familial Dysautonomia) – 183
Stafne’s Bone Defect oftheMandible – 183
Hypertensive Heart Disease – 183
173
4
4.2 Polycystic Kidney Disease – 185
Autosomal Dominant Polycystic Kidney Disease – 185
Autosomal Recessive Polycystic Kidney Disease – 186
Acquired Polycystic Kidney Disease – 187
Di erential Diagnoses andRelated Diseases – 188
4.3 Renal Failure – 188
Examples ofRenal Parenchymal Disorders
According toTheir Anatomical Involvement – 188
© Springer International Publishing Switzerland 2017
J.A. Al-Tubaikh, Internal Medicine, DOI10.1007/978-3-319-39747-4_4
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Chapter 4 · Nephrology
4.1 Hypertension
Hypertension is a disease characterized by an increase in systolic blood pressure >140mmHg and in diastolic blood pressure
>100mmHg. 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.
4
Secondary causes of hypertension include the following:
5 Renovascular diseases : atherosclerosis (adults),
bromuscular dysplasia (children), vasculitis
(polyarteritis nodosa (PAN) and Takayasu arteritis (TA)),
and renal artery aneurysm.
5 Adrenal causes : pheochromocytoma, primary
hyperaldosteronism, and Cushing’s syndrome.
5 Renal parenchymal diseases : chronic glomerulonephritis,
diabetic nephropathy, lupus nephritis, polycystic kidney
disease, and page kidney.
5 Aortic diseases : coarctation of the aorta and midaortic
syndrome.
5 Other causes : brain tumors, congenital AVM, carcinoid
tumors, acromegaly, and hypercalcemia.
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 (
indirect method involves measuring the blood velocity
within the segmental and interlobar intrarenal vessels
(. Fig. 4.1.2 ). The indirect method is insensitive for less
than 60 % RAS.
e 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, gra infections, and obstructive hydronephrosis. e 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 condi-
tion where the kidney is compressed from an adjacent
pathology that causes cortical ischemia. e kidney releases
rennin to overcome the ischemia, leading to renovascular
hypertension.
. Fig. 4.1.1 ). In contrast, the
The Normal Renal Artery Waveform
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
bromuscular dysplasia is the most common cause of renovascular hypertension in children. Atherosclerosis RAS o en
a ects the proximal part of the artery, while bromuscular
dysplasia o en 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 follow-
ing situations:
5 Hypertension in a patient <30years of age or a patient
>50years
5 Hypertension that is resistant to three antihypertensive
regimens
5 Sudden renal functions worsening in a hypertensive patient
5 Sudden development or worsening of hypertension in
any age
5 Unilateral small kidney
5 Renal impairment a er treatment with
angiotensin- converting enzymes (ACE) inhibitors
Parameters
5 The normal renal artery waveform shows low
resistance, continuous profile through the cardiac
cycle, with an RI <0.7. Also, the normal main renal
artery waveform has an early systolic peak (ESP)
(. Fig. 4.1.3 ).
5 e renal-aortic ration ( RAR ) is de ned as the maximum
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 <40cm/s, or aortic PSV >125cm/s. Also,
RAR should not be used in the assessment of renal
artery aneurysm for young patients or patients with
renal artery stents.
5 e normal interlobar and segmental arteries display an
ESP at the beginning of the systole. e ESP is absent
when the arterial stenosis is >60 %. e Doppler angle
should be <30°; otherwise, the peak will not be
demonstrated.
5 e systolic acceleration time ( SAT ) is de ned as the time
measured from the start of the systolic upstroke to the
rst ESP.Normally it is <0.07.
4.1 · Hypertension
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a
175
b
4
. Fig. 4.1.1 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 )
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Chapter 4 · Nephrology
a
b
4
. Fig. 4.1.2 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
Signs of Direct RAS on Doppler Sonography
5 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.
5 Normal RAR (<3.5) and the normal renal PSV
(<180cm/s). Sixty percent RAS shows RAR <3.5,
with PSV between 180 and 200cm/s. There is no
poststenotic turbulence (mosaic pattern/aliasing
artifact) with RAS <60 %. A 60–99 % RAS shows
RAR >3.5, PSV >200cm/s, and poststenotic
turbulence.
Signs on Indirect RAS on Doppler Sonography
5 Absence of the ESP.
5 An accelerated time peak >100ms is consistent
with >60 % stenosis.
5 Tardus parvus waveform consists of slow, damped
systolic acceleration (tardus) and rounding and
flattening of the systolic peak (parvus).
5 More than (−5) difference between the two
kidneys RI.
5 Kidney size <9cm or the difference in size
between the two kidneys >2cm in diameter
(normal kidney size = 9–12cm in diameter).
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