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Review
The Resistive Index in Renal Doppler Sonography:
Where Do We Stand?
Mitchell E. Tublin 1, Ronald O. Bude 2, Joel F. Platt
Technique
Received February 27, 2002; accepted after revision September 19, 2002.
1
Department of Radiology, University of Pittsburgh School of Medicine, 200 Lothrop St., Pittsburgh, PA 15213. Address correspondence to M. E. Tublin.
Department of Radiology, University of Michigan Medical School, 130 Catherine Rd., M4101 MS1, Box 0624, Ann Arbor, MI 48109.
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Tublin et al.
lary pyramids) are then insonated using a 2- to
4-mm Doppler gate. Waveforms should be optimized for measurement using the lowest pulse
repetition frequency without aliasing (to maximize waveform size), the highest gain without
obscuring background noise, and the lowest
wall filter (Fig. 1). Three to five reproducible
waveforms from each kidney are obtained, and
RIs from these waveforms are averaged to arrive at mean RI values for each kidney.
Several studies have shown that a normal
mean renal RI is approximately 0.60. The
largest series to date (58 patients) reported a
mean (SD) RI of 0.60 0.01 for subjects
without preexisting renal disease [37]. Three
prior studies also reported normal mean RI
values of 0.64 0.05 (21 patients) [38], 0.58
0.05 (109 kidneys) [8], and 0.62 0.04 (28
patients) [39]. In general, most sonographers
now consider 0.70 to be the upper threshold
of the normal RI in adults [12, 15]. Important
exceptions to this threshold have been reported, however. In children, it is common
for the mean RI to exceed 0.70 through the
first year of life, and a mean RI greater than
0.70 can be seen through at least the first 4
years of life [40, 41]. In elderly patients
without renal insufficiency, the normal RI
can also exceed 0.70 [42]. It is uncertain
whether this is a normal phenomenon, perhaps due to age-related changes in vascular
compliance, or the consequence of small
vessel changes in the kidney due to aging.
Applications
Obstruction
Most literature on renal Doppler sonography has focused on the potential role of Doppler sonography in the evaluation of ureteral
obstruction. The limitations of the gray-scale
examination for potential acute and chronic
obstruction have been recognized for the past
quarter century. The purely anatomic information that is obtained on sonography may be incomplete or misleading: collecting system
dilatation can be caused by conditions that are
not obstructive (residual dilatation from prior
obstruction that has been relieved, pyelonephritis, and reflux). Also, in the acute setting,
obstruction may be present for several hours
before collecting system dilatation occurs.
In the early 1990s, several groups postulated that the pathophysiology of urinary obstruction might be reliably manifested by
changes in arterial Doppler spectra [2, 5, 8, 9,
15, 17, 25]. This application was based on exhaustive animal research that showed a unique
biphasic hemodynamic response to complete
ureteral obstruction. A short period (<2 hr) of
likely prostaglandin-mediated vasodilatation
occurs immediately after obstruction. After
this period, renal blood flow decreases, and renal vascular resistance increases [4347]. Initial studies suggested that this vasoconstriction
response was primarily mechanical, due to increases in collecting system pressures. Recent
research, however, suggests that complex in-
Fig. 1.Normal resistive index in 25-year-old healthy woman. Color Doppler sonogram is used to identify interlobar artery (arrow); waveform is maximized using lowest pulse repetition frequency possible.
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The lack of specificity of the gray-scale examination in evaluating intrinsic renal disease
has been frustrating to nephrologists and radiologists for decades. Although renal size, corti-
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Tublin et al.
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888
Systolic
Adjustable
height
Diastolic
Function
generator
Solenoid
Pressure
transducer
O2
CO2 Gas
P
F
Data acquisition
computer
Flow
meter
Water
heated to
body temp
Adjustable
height
Stirrer
Pump
Heater
Artery
Ureter
Vein
Kidney
Fig. 3.Diagram of ex vivo pulsatile perfusion system. Perfusion pressures (systole and diastole) are adjusted
by changing heights of reservoirs, and pulse rate is controlled by function generator. Flow (F) and pressure (P)
are measured instantaneously upstream from renal artery using in-line probes. Doppler spectra are simultaneously obtained from perfused kidney using commercially available ultrasound platform. Temp = temperature.
(Reprinted with permission from [94])
0 mm Hg
Ureteral pressure
Systole
Systole
Diastole
Interstitial
pressure
Diastole
Intraarterial
pressure
m Hg
Hg
60 m
0 mm
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60 mm Hg
Ureteral pressure
Fig. 4.Diagram shows how ureteral pressure affects mean, systolic, and diastolic cross-sectional areas of renal arterioles. Area of compliant vessels is determined by transmural pressure (intraarterial pressure interstitial pressure). Interstitial pressure is almost zero in absence of ureteral pressure (left half of diagram). During
diastole, cross-sectional area of vessel is relatively large (B), and some additional distention occurs during systole (A). High ureteral pressures increase interstitial pressure (right half of diagram). In this setting, arteriole is
almost occluded during diastole because transmural pressure is so low (D), but significant distention still occurs
during systole (C). Although mean cross-sectional area is markedly smaller with high ureteral pressures (mean
conductance of C and D, A and B), relative distention that occurs during systole is greater (conductance of A >
B, but C >>D). These cyclic changes in cross-sectional area are underlying cause for parallel changes in total
renal conductance (flow / pressure). (Reprinted with permission from [94])
0 mm Hg
60 mm Hg
Systole
Diastole
Fig. 5.Diagram shows how ureteral pressure affects systolic and diastolic blood flow in larger renal arteries typically insonated during clinical renal Doppler studies.
Each section of figure shows Doppler gate in conduit (segmental or arcuate) artery, which branches into smaller compliant vessels downstream. Length of arrow in Doppler
gate represents velocity of blood flow. As shown in Figure 4, changes in ureteral pressure (0 mm Hg in A and B; 60 mm Hg in C and D) significantly affect arteriolar crosssectional areas and thus total blood flow volume. In less compliant, larger conduit arteries, these changes in blood flow are manifested as cyclic changes in blood velocity.
Thus, relative increase in velocity that occurs at systole (measured using resistive index) is greater when ureteral pressure is elevated (velocity in A > B, but C >> D). (Reprinted with permission from [94])
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Tublin et al.
disease. One might speculate that early reports
of elevated RIs with vascularinterstitial disease
(and not glomerulopathies) were primarily due
to the decreased tissue and vascular compliance
associated with these types of renal diseases
(and not only associated with increased renal
vascular resistance). Later discouraging reports
might be due to differing patient populations
and mixed renal diseases; a single isolated RI
may not be useful in the differential diagnosis of
intrinsic renal disease because of mixed histology and differing effects on vascular compliance and resistance. On the other hand, the
impact of vascular compliance on the RI may
help to explain recent encouraging studies exploring the utility of Doppler sonography in the
assessment of end-organ damage in patients
with hypertension and arteriosclerosis. In several recent studies, an elevated RI was found to
correlate with left ventricular hypertrophy and
carotid intimal thickening [9698].
Conclusion
890
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