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264 A. Frost
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FIGURE 22-10. Normal renal vein: selective right renal
venogram. Note the anastomoses of the venous tributaries
arrows
). (Courtesy of Andrew Kerr, M.D.)
(
FIGURE 22-12. Retrograde male urethrogram: prostatic segment (
arrowhead
cavernous segment (
arrow
).
), membranous segment (
open arrow
), and verumontanum (
curved arrow
black
),
role in dysmotility conditions of the urinary bladder seen
in patients with spinal cord injury (“detrusor-sphincter
dyssynergia”). An investigational technique is being developed to relieve this condition by balloon dilatation of
the external sphincter.
7
The membranous urethra, be-
cause of its location immediately posterior and inferior to
FIGURE 22-11. Normal female urethra: voiding cystogram,
oblique projection; urethra (
), and hymen (
row
open arrow
arrowheads
).
), vaginal reflux (
ar-
the pubic symphysis is susceptible to injury in pelvic fractures.
The third portion of the male urethra is termed the
cavernous urethra and is contained in the corpus spongiosum of the penis. It extends from the external sphincter
to the external meatus. Pathology involving this segment
is related mostly to strictures of various etiologies (posttraumatic, infectious, congenital, or iatrogenic). Classically, the urethral strictures are treated by repeated dilatations or by surgery. More recently, balloon dilatation
and stenting of such strictures have been performed with
good results up to 2 years posttreatment.
7
Uterus
The uterus is a pear-shaped, muscular organ located in
the female pelvis. It is attached inferiorly to the fornix of
the vagina and lies between the urinary bladder anteriorly and the rectum posteriorly.
The arterial supply to the uterus is constituted by the
uterine arteries, which are branches of the right and left
internal iliac arteries. The uterine arteries divide into
ascending and descending branches, which course alongside the lateral aspect of the uterus, within the myometrium. The ovarian arteries, which are direct branches of
the abdominal aorta, also supply the uterus and anastomose with the branches of the uterine arteries. The venous drainage of the uterus originates in a plexus around
the cervix from which branches paralleling the uterine
arteries extend into the broad ligament and drain into
the iliac veins. Anastomoses between the uterine venous
8
Anatomy of the Kidneys and Genitourinary Tract 265
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plexus and the superior rectal vein contribute to portosystemic anastomoses.
Uterine tubes
The uterine (fallopian) tubes are paired, approximately
10 cm long tubular structures, located on the right and
left sides of the uterus. Each tube extends from the level
of its respective uterine cornu to the pelvic peritoneum
in the vicinity of the ipsilateral ovary. A direct communication is thus established between the peritoneal cavity
and the exterior, through the endometrial cavity, the
cervical canal, and the vagina (Fig. 22-13).
On hysterosalpingography, the uterine tube has four
segments.
8
The intramural segment is the part of the tube
contained within the myometrium and extending from
the uterine ostium to the lateral aspect of the wall of the
uterus. The isthmus is the narrowest segment of the tube
and has the thickest wall. It extends for a length of 2 to 5
cm laterally to the intramural segment and is continued
by the ampulla, which is the widest and longest segment
of the tube and the site where fertilization of the oocyte
takes place. The infundibulum, the funnel-shaped lateral
segment of the tube, contains the abdominal ostium,
which is surrounded by digitations called fimbriae. The
uterine tubes are intraperitoneal (being contained in the
cranial edge of the broad ligament) and therefore are
FIGURE 22-13. Normal hysterosalpingogram, left anterior
projection; note the plicae palmatae of the cervix (
the internal cervical os (
flexed uterine body with triangular appearance of the endometrial cavity, and patency of both uterine tubes with pooling
of contrast in the peritoneal cul-de-sac (
refluxed into the formix of the vagina, outlining the vaginal
segment of the cervix (
open arrow
black arrow
), anteverted and ante-
).
9
white arrow
arrowhead
). Contrast
relatively mobile. The arterial supply and the venous
drainage derive from anastomoses between uterine and
ovarian vessels.
Female infertility can be caused by tubal occlusion. A
promising development in interventional radiology is the
selective retrograde catheterization of the tubes, for both
diagnostic and therapeutic purposes (see Chapter 27).
■ Congenital Anomalies of Relevance
to the VIR
A full discussion of urological and reproductive congenital anomalies is beyond the scope of this chapter. The
following is a brief analysis of the relevance of some of
these anomalies to the VIR.
Many of the congenital anomalies result in urinary obstruction and infections, with or without renal failure,
especially in the pediatric age group. In older patients,
stone formation can complicate many of these conditions. Uroradiologic inter ventions are required for the
diagnosis and treatment of these conditions and their
secondary complications; these interventions are detailed
in Chapter 24. Examples of such congenital anomalies
are: ureteral multiplications (sometimes associated with
ectopic implantation of the ureter and ureterocele), various forms of renal fusion (most frequent of which is the
horseshoe kidney), renal ectopia (particularly the pelvic
kidney), retrocaval ureter, megaloureter, ureteral stenosis, diverticula (caliceal, ureteral, or urethral), and urethral valves.
Other congenital anomalies present with hematuria
and require diagnostic or therapeutic radiological renovascular procedures. Examples of such conditions are
congenital aneur ysms, congenital arteriovenous fistulae,
and the “nutcracker syndrome” (i.e., compression of the
left renal vein between the aorta and the mesenteric
vessels, with increased pressure in the left renal vein and
formation of peripelvic and periureteral varices)(see
Chapter 23).
A causal relationship was proved between varicocele
and male infertility. Varicoceles are related to developmental abnormalities of spermatic vein valves. Transcatheter embolization of varicocele is now an established
procedure (Chapter 27).
Certain congenital anomalies impede interventional
access or require modification of standard interventional
techniques. For example, percutaneous nephrostomy access can be difficult in horseshoe, ectopic (crossed or
),
uncrossed, fused or unfused), or malrotated kidneys. Percutanous insertion and positioning of inferior vena cava
filters, venous catheterization, and blood sampling may
be influenced by the presence of anomalies such as multiple renal veins, circumaortic renal veins, and double or
left-sided inferior vena cava (see Chapters 19 and 27).
11–12
10
13
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Finally the presence of certain anomalies or normal
variants must be documented before surgical inter ventions are performed. For example, aberrant or accessory
renal arteries must be identified before repair of abdominal aortic aneurysm or renal transplant donor nephrectomy. The preoperative evaluation of the renal transplant
donor is discussed in Chapter 23.
REFERENCES
1. Davidson AJ. Radiologic anatomy of the kidney. In: Radiology of the
kidney. Philadelphia: WB Sauders, 1985;71–88.
2. Castaneda-Zuniga WR, Tadavarthy SM, Hunter DW. Percutaneous
uroradiologic techniques. In: Castaneda-Zuniga WR, Tadavarty SM,
eds. Interventional radiology, 2nd ed. Baltimore: Williams & Wilkins,
1992:777–787.
3. Preminger GM, Schulz S, Clayman RV, et al. Cephalad renal movement during percutaneous nephrostolithotomy. J Urol 1987;137:
623.
4. Meyers M. The extraperitoneal spaces; normal and pathologic anatomy. In: Dynamic radiology of the abdomen: normal and pathologic anat-
omy. New York: Springer-Verlag, 1976:113.
5. Netter FH. Kidneys, ureters and urinary bladder. In: Shapter RK,
Youkman FF, eds. The CIBA collection of medical illustrations, 4th ed.
West Caldwell: CIBA, 1987:2–4.
6. Castaneda F, Hunter DW, Amplatz K, et al. Retrograde transurethral prostatic urethroplasty with balloon catheter. In: Castaneda-
Zuniga WR, Tadavarty SM, eds. Interventional radiology, 2nd ed. Baltimore: Williams & Wilkins, 1992:1015–1027.
7. Castaneda F, Brady TM, Bertino RE, et al. Other lower urinary tract
interventions. In: Castaneda-Zuniga WR, Tadavarty SM, eds. Inter-
ventional radiology, 2nd ed. Baltimore: Williams & Wilkins, 1992:
1034–1042.
8. Moore KI. The perineum and pelvis. In: Clinically oriented anatomy, 2nd ed. Baltimore: Williams & Wilkins, 1985:373–380.
9. Gray H. The urogenital system. In: Clemente CD, ed. Anatomy of the
human body, 30th ed. Philadelphia: Lea and Febiger, 1985:
1571–1576.
10. Thurmond AS. Fallopiantube catheterization for improved diagnosis and treatment of proximal tube obstruction. In: CastanedaZuniga WR, Tadavarty SM, eds. Interventional radiology, 2nd ed. Baltimore: Williams & Wilkins, 1992:1046–1051.
11. Kunnen M, Cornhaire F. Nonsurgical cure of varicocele by transcatheter embolization of the internal spermatic vein(s) with a histoacryl tissueadhesive. In: Castaneda-ZunigaWR, Tadavarty SM, eds.
Interventional radiology, 2nd ed. Baltimore: Williams & Wilkins,
1992:73.
12. Herrera MA, Di Segui R, Kaye KW, et al. Embolization of the
internal spermatic vein with mechanical devices for the treatment
of varicocele. In: Castaneda-Zuniga WR, Tadavarty SM, eds. Inter-
ventional radiology, 2nd ed. Baltimore: Williams & Wilkins, 1992:101.
13. Herrera MA, Tadavarty SM, Yedlicka JW et al. Inferior vena cava
filters. In: Castaneda-Zuniga WR, Tadavarty SM, eds. Interventional
radiology, 2nd ed. Baltimore: Williams & Wilkins, 1992:666.
J.J.TrambertVascular Manifestations of Renal Disease
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23
■■■
Vascular Manifestations
of Renal Disease
JONATHAN J. TRAMBERT
This chapter deals with diseases of the kidneys for which
angiography or percutaneous transcatheter vascular interventional procedures play a major role. Nonneoplastic
entities are discussed first.
■ Renovascular Hypertension
The interventional radiologist often is called on to help
diagnose or treat renovascular hypertension. Renovascular hypertension is hypertension that is caused by arterial
inflow reduction, which in turn causes renal ischemia and
a secondary increased renin production. The mechanism
of renovascular hypertension is believed to be as follows.
When blood flow to the kidneys is limited to the point that
it causes renal ischemia, glomerular filtration pressure
drops, resulting in decreased filtration of blood by the
kidney. Cells in the juxtaglomerular apparatus are stimulated to secrete renin, which causes elevation of the blood
pressure, increasing the perfusion to the ischemic kidney,
correcting the ischemia, and increasing the glomerular
filtration pressure. The physiologic mechanism of renovascular hypertension is summarized in Figure 23-1.
It must be kept in mind that hypertension related to
excess renin secretion can have other causes. For example, it can be the result of chronic renal inflammation,
which results in renal parenchymal insufficiency, or,
rarely, a renin secreting tumor (a reninoma or juxtaglomerular tumor).
1
Etiology of renal artery occlusive disease
Renal artery occlusive disease can result from several
disease processes. The two most common causes of reno-
vascular hypertension are atherosclerosis and fibromuscular dysplasia (FMD).
Atherosclerosis is the most common cause of renovascular hypertension, accounting for approximately 60% of
such cases.
over 50 years. A relatively large percentage (37%) of
patients with atherosclerotic renovascular hypertension
will have bilateral renal artery stenosis.
sclerotic renal artery stenoses are located in the proximal
third of the renal artery and frequently involve the renal
artery origin secondar y to overhanging aortic mural atherosclerotic plaques (Fig. 23-2). This pattern of disease is
relevant to the efficacy of balloon angioplasty in treating
atherosclerotic renal arter y stenosis.
FMD is the cause of renal artery stenosis in approximately one third of patients with renovascular hypertension.
tend to occur in children and young adults, and the lesion
tends to affect the mid to distal main renal artery and in
some cases its branches. Branch vessel disease is quite
common in FMD-induced renovascular hypertension in
children. There are several types of FMD based on their
pathology (Table 23-1).
countered in practice is medial fibroplasia, which is
caused by areas of circumferential medial thickening alternating with areas of aneurysm formation. Angiographically, this type manifests as a “string of beads” appearance
(Fig. 23-3).
Other less common causes of renovascular hypertension include chronic aortic dissection with impingement
on the renal artery ostium by the intimal flap, aortoarteritis such as Takayasu’s disease, neurofibromatosis, renal
artery aneurysm, atheromatous and cholesterol emboli,
postoperative stenosis at a previous bypass graft anast-
2
Most patients are older men, usually aged
3
Most athero-
2
Unlike atherosclerotic stenoses, stenoses of FMD
2
The most common variety en-
267
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FIGURE 23-1. Physiologic mechanism of hypertension.
FIGURE 23-2. Bilateral atherosclerotic proximal renal artery
stenoses: moderate on left, severe on right. Note the diffusely
diseased abdominal aorta and prominent plaque immediately
superior to right renal artery ostium (
arrow
).
TABLE 23-1.
Type (%) Angiographic findings
Medial fibroplasia 60–70 “String of beads” caused
Perimedial fibroplasia 15–25 Chain of irregular stenoses
Medial hyperplasia 5–15 Long, smooth narrowing
Medial dissection 5 False channel, aneurysm
Intimal fibroplasia 1–2 Short, focal stenosis
Adventitial fibroplasia ⬍1 Long, segmental stenosis
From Kadir S. Diagnostic angiography. Philadelphia: WB Saunders, 1986:459.
Categories of fibromuscular dysplasia
Prevalence
by focal stenosis alternating
with aneurysmal dilatation
without aneurysms
omosis or renal transplant artery anastomotic stenosis,
and coarctation of the aorta with renal artery stenosis.
4
Diagnosis
Of the entire hypertensive population, fewer than 5%
will have renovascular hypertension. The remaining 95%
have essential hypertension, which is not attributable to
any specific anatomic abnormality and thus is treatable
only by long-term medication. Long-term medication for
hypertension often involves multiple medications that
have possible side effects. For this reason, detection of
a correctable anatomic abnormality is a desirable goal.
Initially there was a great deal of enthusiasm for screening all hypertensive patients for renovascular hypertension, but, given the low prevalence of renovascular hypertension, even with a test of moderately good sensitivity
and specificity, the frequency of false-positives equals or
exceeds the frequency of true-positives.
nations, although capable of diagnosing renal artery
stenosis as the cause of a patient’s hypertension with a
higher degree of certainty, are not appropriate as screening examinations because of their cost and morbidity.
These problems led to the abandonment of indiscriminate screening for renovascular hypertension.
The current approach to screening patients for renovascular hypertension involves screening only those hypertensive patients who, based on clinical parameters, are
most likely to have renoocclusive disease as an etiology.
These parameters include abrupt onset of hypertension
before age 30 or after age 55, severe hypertension (diastolic blood pressure greater than 120 mm Hg), accelerated or malignant hypertension with retinopathy, hypertension refractory to triple-drug therapy, epigastric
bruit, moderate hypertension with unexplained azotemia, and azotemia induced by angiotensin-converting enzyme (ACE) inhibitors.
6
Radionuclide renography, Doppler ultrasound velocity
measurements, and Doppler renal-resistive index measurements are among the noninvasive modalities used in
the diagnosis of renovascular hypertension. Each modal-
5
Invasive exami-
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FIGURE 23-3. Fibromuscular dysplasia, medial fibroplasia
type, of right renal artery. Note the “string of beads” appearance
of the main artery.
ity has its limitations, but each also has some value in
screening carefully selected persons.
7–9
Magnetic resonance angiography
Magnetic resonance angiography (MRA) shows great
promise as a noninvasive modality for visually depicting
the renal arteries and aorta. The available types of image
acquisition techniques include two-dimensional (2-D)
time-of-flight (TOF), 2-D or 3-D phase-contrast, and 3-D
TOF, with or without intravenous gadolinium. The goal of
MRA acquisition is to suppress signal from surrounding
nonvascular structures and either to enhance or at least
limit the suppression of flowing blood signal, which, in effect, produces a “subtraction arteriogram.” The resultant
image data set can be reconstructed in a 3-D image depiction that can be rotated and viewed from multiple angles.
MRA is reasonably sensitive and specific in depicting
the aorta and proximalrenal arteries. It is less sensitive for
defining the distal main renal artery or beyond the division points of the main renal artery.
10,11
Renal MRA has
proved extremely valuable in the evaluation of the patient
in whom there is a reasonable clinical suspicion of renovascular hypertension but in whom renal insufficiency
poses a relative contraindication to contrast arteriography. A negative MRA virtually excludes a central renal
artery lesion as the cause of the hypertension or the cause
of acute onset of renal insufficiency (Fig. 23-4).
Spiral CT angiography
Spiral computed tomagraphy angiography (CTA) also
holds promise as a modality for evaluating the renal ar-
FIGURE 23-4. Magnetic resonance angiogram (MRA) of normal
proximal renal arteries (
rowheads
sity projection (MIP) constructed
from a three-dimensional phasecontrast intravenous MRA using
gadolinium. Other structures depicted on this MIP are the superior
mesenteric artery (SMA) (
row
rior vena cava (IVC) (
rows
portal vein (
). Axial maximum inten-
), left renal vein joining the infe-
), and splenic vein joining the
large white arrows
white ar-
black ar-
small white ar-
).
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J.J. Trambert
teries because of its relative noninvasiveness compared
with catheter arteriography. The premise behind CTA is
the rapid acquisition of axial images in the areas of interest in a single breath-hold, made possible by slip ring
technology. The axial images can be reconstructed into a
3-D model of the arterial system that can be viewed from
different angles.
12
The disadvantage of CTA is the need
for intravenous iodinated contrast, which limits its usefulness in certain patient populations, especially in patients
with renal insufficiency or renal transplant artery
stenosis. Often the amount of contrast needed for CTA
far exceeds that required for a properly performed catheter arteriogram.
Contrast arteriography
Contrast arteriography is still the gold standard when it
comes to anatomic detection of a renal arter y stenosis;
however, finding a renal artery stenosis in a hypertensive
patient does not necessarily mean that the patient has
renovascular hypertension. The renal artery arteriosclerotic lesion may be a consequence of the long-standing
essential hypertension rather than a cause of it, or it may
be totally unrelated. Furthermore, a significant percentage of patients who were found to have a renal artery
stenosis at autopsy had been normotensive.
13
Renal arteriography technique
When performing renal arteriography, a nonselective
aortogram almost always is obtained first. The aortogram
discloses the number of renal arteries supplying each
kidney, the relative location of the renal arteries and
kidneys, the origins of the renal arteries, and the aorta.
When considering intervention for renovascular hypertension, the aortogram should be tailored to assess the
celiac artery and its branches; in the event that surgical
bypass is needed for treatment, these arteries frequently
are used for inflow. The information on the aortogram
facilitates the performance of selective renal arteriography and interventions, because without it, locating the
renal artery orifice for selection may be more difficult
and time consuming, accessory renal arteries may be
missed, and renal artery origin disease may go undetected by a more distal selective catheter injection. Indeed, selective renal arteriography may not be needed in
the evaluation of suspected renovascular hypertension if
the aortogram clearly discloses a proximal renal arter y
stenosis or renal artery occlusion.
If the aortogram fails to disclose a lesion in a patient in
whom there is a high suspicion of renovascular hypertension based on clinical history and noninvasive studies,
selective renal arteriography must be performed. Transcatheter pressure gradient measurements can be helpful.
Branch artery stenosis can be the cause of renovascular
hypertension especiallyin children, and can be difficult to
detect on nonselective aortography. Renovascular hypertension secondary to a distal branch artery stenosis can
occur in FMD and less commonly in atherosclerotic disease. Specifics regarding technique and performance of
aortography, selective vessel catheterization, angiographic contrast injections, and image acquisition are discussed in Chapter 2.
If arteriography discloses a significant renal artery stenosis, corroborated by clinical history, laboratory findings, and noninvasive studies, percutaneous transcatheter
therapy can be initiated in the same session in selected
patients.
Renal vein renin assay
Renal vein renin assay directly measures and compares
the renin output of each kidney. It reflects the pathophysiology of renovascular hypertension. Combined with
noninvasive modalities or angiographic detection of renal artery stenosis, renal vein renin assay increases the
likelihood of confirming the presence of a lesion whose
treatment will cure or improve the hypertension.
Blood samples are drawn from each renal vein and
from the inferior vena cava below and above the renal
veins. Care should be taken to ascertain whether any
accessory renal veins are in the area. Also, whenever
possible, the left renal vein sample is drawn peripheral to
the gonadal vein to minimize dilution by nonrenal blood.
Usually, a cobra-shaped catheter is used to select the
renal veins. Peripheral selection of the left renal vein can
be facilitated by the use of a tip deflector wire when
necessary. To minimize the risk of blood aspiration impedance from the catheter tip invaginating the vein wall,
a single side hole is punched in the catheter within 1 to
2 mm of the tip. Contrast injection is minimized because
it can adversely affect the renin output measurements.
Before blood samples are drawn, approximately 3 to 4
mL of blood in the catheter should be aspirated and
discarded. Then approximately 5 mL of blood is slowly
aspirated (to avoid causing excess turbulence in the
blood flow during aspiration), and samples are placed on
ice immediately to preser ve them on route to the radioimmunoassay laboratory. Each sample must be meticulously labeled, and each sample location should be
indicated on a vein diagram to allow exact correlation
between assay levels and vein location.
The accuracy of renal vein renin sampling is diminished in patients with renal insufficiency, long-standing
hypertension, and bilateral renal artery stenosis and also
by the administration of antihypertensive medications
during the assay. The ratio of renin levels of the two renal
veins must be greater than 1.5:1 to be considered significant. A more complicated but more specific method for
the use of renin levels in predicting the therapeutic re-
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sponse to the treatment of renal artery stenosis has been
reported.
14
Treatment
Before the advent of percutaneous transluminal balloon
angioplasty (PTA), surgical bypass and endarterectomy
were the only treatment options for renovascular hypertension. PTA has revolutionized the treatment of renal
artery stenosis. Surgical bypass is still indicated in some
patients with relative contraindications to renal PTA. Furthermore, surgical bypass is still an option for patients
who fail to respond to renal PTA or who develop complications of PTA that are not correctable with percutaneous transcatheter measures.
In addition to the risk of general anesthesia, potential
surgical morbidity includes renal failure, with a significant risk of cholesterol emboli related to cross clamping
of a severely calcified atherosclerotically diseased aorta.
The perioperative mortality rate is 2 to 4%.
15
Successful
surgical reconstructions have a somewhat better longterm primary patency than renal PTA, but the far greater
morbidity and mortality of operative repair mitigate in
favor of using PTA as the initial treatment, with surgery
reserved for those patients who fail renal PTA or who
have relatively strong contraindications to PTA.
16
Percutaneous transluminal angioplasty
Pharmacologic aspects
Because of the chance of therapeutic benefit of postrenal PTA with a resultant precipitous drop in blood
pressure, the patient’s antihypertensive medications must
be appropriately adjusted. Long-acting antihypertensive
medication must be discontinued prior to renal PTA;
short-acting drugs (e.g., intravenous nitroprusside)
should be substituted. One must be prepared to administer vigorous intravenous hydration to increase vascular
volume in the event of a significant post-renal PTA blood
pressure drop.
Risks of renal PTA include thrombosis and small artery branch spasm induced by catheter-guidewire manipulations. The risk of vasospasm can be minimized by
administering an antispamodic drug at the outset of the
procedure, such as a calcium channel blocker (e.g.,
nifedipine 10 mL sublingual). It is also essential to
heparinize the patient therapeutically to minimize the
risk of thrombosis. Doses for heparin range from 3,000
to 10,000 units, and adequacy of anticoagulation can be
monitored by obtaining activated clotting times in the
angiography suite. Low-dose aspirin (325 mg/day), beginning the day before and continuing for 6 months
following PTA, also is advised by most practitioners to
decrease the risk of post-PTA thrombosis and possibly
the risk of restenosis.
Technique
After suitable angiographic evaluation of the renal artery
stenosis, the affected renal artery is selected. Renal artery
PTA necessitates the advancement of aguidewire well into
the peripher y of the renal arterial tree to ensure secure
access across the stenosis for balloon advancement, which
usually can be accomplished by using conventional selective catheters such as the cobra or simple C-shaped curve.
In situations where the affected renal artery possesses a
caudal angulation or where there is a very tight stenosis,
conventional selective catheter shapes may not permit
guidewire advancement across the stenosis or sufficiently
peripheral guidewire advancement to allow catheter exchanges and balloon placement. In such a situation, use
of a downward curving catheter such as a sidewinder,
Simmons, or“shepherd’s crook” shape often can facilitate
superselective secure catheterization. The advantage of
the sidewinder curve in this circumstance is that withdrawing the catheter at the femoral puncture site will
advance the catheter tip across the tight stenosis or into
the downward angling renal artery with a force that is not
obtainable with conventional cobra or simple C-shaped
catheters.
17,18
Tominimize the risk of arterial dissection, it
is important that catheter advancement across the renal
artery stenosis be performed using a soft-tipped
guidewire such as a Bentson (Cook Incorporated, Bloomington, IN) or TAD II (Mallinckrodt, St. Louis, MO) or
during simultaneous contrast injection that will keep the
tip off of the wall. A less commonly used approach for
downward angling renal arteries is the axillary puncture.
After a catheter has been advanced securely into the
renal artery, a guidewire must be advanced sufficiently
peripherally into the renal arterial tree to permit safe
catheter exchange and balloon advancement. The ideal
guidewire has a short, floppy atraumatic end with rapid
transition to a robust stiff section. The short soft tip is
important to minimize the risk of trauma in the renal
artery branch in which the wire is anchored, but it is important that the section of wire bridging the stenosis be
stiff enough to guide the balloon successfully. A commonly used wire is the Rosen wire, which possesses these
properties. There is controversy as to whether the guidewire tip should possess a tight 1.5 mm radius “J” or be
straight. The advantage of the “J” tip is that the tip presents
a blunt end that is less likelyto perforate a peripheral renal
artery branch. The disadvantage of the “J” tip wire is that
when it is wedged into an artery branch smaller in diameter than the radius of the “J,” it can induce vasospasm, a
problem that is avoided when using a straight tip.
Intraarterial nitroglycerine should be administered immediately prior to superselective catheterization of the
peripheral renal artery branches to minimize the risk of
vasospasm. Nitroglycerine is effective and has a short
half-life, allowing for administration of repeat doses (50
to 200 lg).
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After the guidewire has been advanced into a peripheral renal artery branch, the balloon is advanced across
the stenosis (Fig. 23-5). Balloon size is chosen based on
the measured size of the adjacent “normal” renal artery
on the angiogram. The balloon used for renal PTA should
have a short length and short distance between the balloon’s distal end and the catheter tip. This configuration
will minimize “torquing” of the renal artery with respect
to the aorta as the balloon inflates and tries to straighten.
Other catheter guidewire combinations that can be
A B
FIGURE 23-5. Renal artery angioplasty. A: Aortogram show-
ing severe proximal right renal artery atherosclerotic stenosis
(same patient as in Fig. 23-1) before angioplasty. B: Balloon
being inflated across stenosis (note waist). C: Right renal
arteriogram after angioplasty using sidehole catheter demon-
C
strating good lumen response to angioplasty.
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used to facilitate successful treatment of difficult renal
lesions include hydrophilic balloon catheters to decrease
friction, miniature low-profile balloon catheters such
as the 3.8 Fr Medi Tech sub-4 balloons, and a balloon
mounted on a guidewire (Teg wire, Medi Tech Inc.). The
performance of renal PTA also can be facilitated by using
an outer guiding catheter positioned at the renal artery
orifice through which the balloon is advanced, allowing
test injection of contrast with the balloon or guidewire
still across the stenosis.
Just as with extremity PTA, it is essential to evaluate the
result of renal PTA while access is maintained across the
newly treated stenosis. If a guiding catheter is used, contrast can be injected through it. My preference is astraight
or simple curve catheter with side holes placed along
its distal few centimeters. After renal PTA, this catheter
is placed across the treated lesion, allowing contrast injection to opacify the entire renal artery out to the aorta
and allowing assessment of the result of renal PTA (see
Fig. 23-5). If necessary, the guidewire can be readvanced
through the catheter to allow additional manipulations as
needed.
Complications
Besides vasospasm and arterial thrombosis, other complications of renal PTA include cholesterol or atheroemboli, renal artery rupture, acute renal artery occlusion
resulting from dissection, and renal failure. Cholesterol/
atheroemboli is an occasional and feared complication
that can cause peripheral end-artery occlusions and potentially segmental or diffuse renal infarction. Unfortunately, anticoagulation cannot prevent this type of embolization, and thrombolysis does not reverse it. The risk
is much higher in patients who have extremely diseased
aortas with ulcerated and irregular plaques.
Renal artery rupture is an uncommon occurrence, but
the risk of rupture is minimized by proper balloon sizing.
Angiographic measurements of vessel size result in a 15
to 20% overestimation of vessel size from magnifica-
18
tion.
This slight overdistenstion is desirable to maximize the chance of successful plaque dehiscence and
durable stenosis dilation. Larger balloons should be used
with extreme caution, and the onset of severe pain during
balloon inflation is probably an indication that the balloon is too large, risking renal artery rupture. Persistence
of pain after the balloon is deflated may indicate that
rupture has occurred. If rupture is suspected, a quick
confirming contrast injection should be performed and
the balloon should be inflated across the arterial breach
to tamponade it temporarily while awaiting definitive surgical repair. Future availability of covered stents may allow
percutaneous treatment of such ruptures. Acute occlusion of the renal artery caused by dissection now can
sometimes be treated with renal artery expandable wire
mesh stents but occasionally requires urgent reconstructive surgery.
Post-renal PTA renal failure can occur because there is
a certain minimum amount of contrast that must be used
to guide the procedure and to evaluate the result. For this
reason, it is advisable to limit the amount of contrast used
to the minimum necessary, to use nonionic contrast, and
to wait at least 2 days between diagnostic arteriography
and arterial intervention in patients with renal insufficiency to minimize the risk of cumulative contrast load to
the kidneys.
19
Renal PTA should be performed only in situations
where skilled vascular surgery backup is available on short
notice. The absence of skilled vascular surger y backup
should be considered a contraindication to the performance of renal PTA, because some of the potential complications can only be treated surgically and must be done
expeditiously. Acute renal artery occlusion secondary to
dissection sometimes can be treated by placement of a
stent.
Renal artery thrombosis can be treated by intraarterial
thrombolysis. Nonetheless, one must be aware that, unlike the arteries of the lower extremities, the renal artery
is an end vessel, and hence renal artery occlusion results
in renal ischemia that cannot be tolerated for a long
period. Another relative contraindication to renal PTA is
the presence of an extremely diseased irregular aorta in
which the risk of cholesterol or atheroemboli is relatively
high.
Results
The ultimate result of renal PTA depends on the successful revascularization of the renal artery and subsequent
amelioration of the hypertension and improvement in
the renal function. Martin et al.
19
reviewed the renal artery PTA literature and determined that PTA of atherosclerotic lesions results in cure in 13% and improvement
in 52%. Renal artery PTA for FMD, on the other hand,
results in cure in 44% and improvement in 45% of cases.
Cure is defined as reduction of diastolic blood pressure to
90 mm Hg or lower, without the need for medications.
Improvement is defined as a 15% reduction in diastolic
blood pressure to a value between 90 and 110 mm Hg.
The reason why the cure and benefit rate is higher
for FMD than for atherosclerotic renal artery stenosis
probably relates to demographics and overall clinical
status of the patients involved as well as to the usual
morphology of the respective lesions. Atherosclerotic
renal artery stenosis usually occurs in association with
other manifestations of atherosclerosis, such as coronary
artery disease, peripheral vascular disease, and cerebral
vascular disease. Many of these patients are older, with
chronic concomitant essential hypertension and some
element of nephrosclerosis related to these factors.
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