2. NORMAL RENAL ARTERIAL ANATOMY
• Originate from the lateral sides of the aorta
at the level of the superior border of the second lumbar vertebra
directed slightly anteriorly usually 1-2 cm below the superior mesenteric
artery origin.
The right RA originates from the anterolateral aspect of the aorta and
immediately turns posteriorly to course beneath the inferior vena cava (IVC).
The left RA originate from the posterolateral surface of the aorta and
courses posteriorly the surface of the aorta and over the psoas muscle.
3. • The main renal artery divides into
segmental arteries near the renal
hilum .
• The first division - posterior branch,
which arises just before the renal
hilum and passes posterior to the
renal pelvis .
• At renal hilum anterior branch devids
in to apical, upper, middle, and lower
anterior segmental arteries.
• The apical and lower anterior
segmental arteries supply the
anterior and posterior surfaces of the
upper and lower renal poles,
respectively
• the upper and middle segmental
arteries supply the remainder of the
anterior surface.
4. RENAL ARTERY STENOSIS
Most common cause of secondary hypertension deteriorating renal function.
CAUSES
atherosclerotic disease
fibromuscular dysplasia
arteritis (polyarteritis nodosa,Takayasu's disease)
Thromboembolic, arterial dissection, infrarenal aortic aneurysm, post
radiation.
compression of the renal artery by retroperitoneal masses.
Pheochromocytoma.
5. PRESENTATION
•Very high or sudden increase in blood pressure in the child or adult.
•hypertension that is difficult to control with medication
•Epigastric or flank bruit
•Unexplained impairment of renal function
•presence of coronary and peripheral arterial disease, and flash pulmonary
edema.
6. IVU
The affected kidney small and smooth
The reduced perfusion on the affected side produces a late nephrogram
giving rise to a hyperdense nephrogram.
Similarly there is late appearance of contrast into the pelvicalyceal system
and again this becomes hyperdense.
Notching of the ureter due to compensatory hypertrophy of the ureteric
artery .
7. CAPTOPRIL SCINTIGRAPHY
The mean transit time is prolonged
Diminished uptake
Flattened peak and delayed Tmax.
In severe cases the clearance may be so slow that the curve continues rising
throughout the period of observation.
•Grade I Mild delay in Tmax (6-11 min) with a falling excretion phase
•Grade 2a More prolonged delay in T max (greater than 1 1 min) but still with an
excretion phase
•Grade 2b Continually rising or flat curve
Grade 3 As grade 2b, with marked reduction in function of the affected kidney.
8. ULTRASOUND
first step in the investigation
It is a simple non-invasive
And exclude an obvious structural abnormality or coexistent condition that
may relate to the hypertension (renal scarring, hydronephrosis, calculus
disease and rarely renal or adrenal tumours )
Obvious size disparity b/w the two kidneys (2cm)
One kidney is abnormally small – s/o unilateral RAS
9. DOPPLER CRITERIA FOR DIAGNOSIS OF RAS
Doppler US criteria of RAS can be divided into two groups based on
•Direct findings obtained at the level of the stenosis (proximal criteria)
•Flow changes observed in the renal vasculature distal to the site of stenosis
(distal criteria).
10. PROXIMAL CRITERIA (DIRECT EVALUATION OF THE STENOSIS)
Four criteria are used to diagnose significant proximal stenosis or occlusion of
the RA.
The first and most important sign is the increase in PSV.
Velocities higher than 180 cm/s suggest the presence of a stenosis of more
than 60%
End-diastolic velocity greater than 150 cm/s suggests a degree of stenosis
greater than 80%.
11. The second criterion is the comparison of PSV values obtained in the prerenal
abdominal aorta with those measured in the RAs, the so-called renal/aortic
ratio (RAR)
In normal conditions, RAR is lower than 3.5.
If PSV obtained in the prerenal abdominal aorta is abnormally low (less than
40 cm/s), RAR cannot be used.
The third criterion is identification of RAs with no detectable Doppler signal, a
finding that indicates occlusion.
The fourth criterion is the visualization of color artifacts such as aliasing at the
site of the stenosis and the presence of turbulence at Doppler evaluation
indicating the presence of a significant stenosis.
12. DISTAL CRITERIA (INDIRECT EVALUATION OF THE STENOSIS)
Waveform alterations distal to the stenosis in arterial segments (hilar or
interlobar arteries).
loss of early systolic peak
acceleration index (AI) lower than 3 m/s2;
acceleration time (AT) > 0.07 s
a difference between the kidneys in RI > 5% or
in pulsatility index >0.12.
“tardus–parvus” effect.
A great difference in RI values obtained on the 2 kidneys (>0.05–0.07) is
another criterion for diagnosis of RAS .
13.
14. Criteria for the classification of RA stenosis by color-Doppler US from Zieler
and Strandness (Am J Hypertens, 1996).
Renal artery diameter reduction Renal artery PSV RAR
Normal <180 cm/s <3.5
<60% >180 cm/s <3.5
≥60% >180 cm/s ≥3.5
Occlusion No signal Indeterminable
15. ANGIOGRAPHIC FINDINGS:
CTA and MRA following bolus I.V injection of contrast medium
Atherosclerotic lesion
Focal / segmental, eccentric or concentric stenosis
Location: ostium or proximal 2cm of renal artery
Unilateral or bilateral calcifications
Fibromuscular hyperplasia
Focal concentric narrowing of distal main RA and intra renal branches
Narrowing of the affected vessel with a “string of beads” or nodular
appearance
16.
17. Interventional radiology in the treatment of renal artery stenosis
Percutaneous transluminal renal angioplasty (PTRA) alone or in
combination with stent implantation
18. SELECTING PATIENTS FOR RENAL REVASCULARISATION
Refractory hypertension on multidrug regimen.
Progressive azotemia.
ARF on ACE inhibitors in patients with CHF
Recurrent flash pulmonary oedema
Bilateral renal artery stenosis or stenosis of renal artery supplying single
functioning kidney.
Salvage therapy in recent onset end stage renal failure (preserved renal
size and parenchymal thickness)
19. DIFFERENTIAL DIAGNOSIS
ARTERIAL DISSECTION
Aortic dissection extending in to the renal artery.
Frequently seen in elderly people.
CT/ANGIO
•Irregular caliber of aortic lumen
•False or occluded lumen and intimal flap.
•Thickened aortic wall.
•Narrowing or occlusion of renal artery due to false lumen of dissection.
may occlude or narrow renal artery at its origin
may extend in to renal artery producing more distal narrowing
MR
Demonstrate aortic dissection with intimal flap with extension to renal
arteries.
20. VASCULITIS
POLYARTERITIS NODOSA AND TAKAYASU ARTERITIS:
•Inflammation of the medium to large arteries.
•Fibrous thickening of the wall of the aorta, narrowing orifices of the major
branches.
Other D/D
Extrinsic compression of renal artery caused by
•Abdominal aortic aneurysm
•Retroperitoneal tumors
•Retroperitoneal fibrosis
The segmental arteries then course through the renal sinus and branch into the lobar arteries.
Further divisions include the interlobar, arcuate, and interlobular arteries.
Hyper dense nephrogram due to more concentrated urine on the affected side compared to opposite side
Normal renal artery wave form
Tardus means slow and late and parvus means small and little. Slow rise of systolic wave or delay in the rise of systolic wave
Sting of beads due to focal annular repetitive intimal and medial proliferative changes in fibromuscular dysplasia
used as an alternative technique to surgical revascularization