Skip Navigation


NDT Advance Access originally published online on December 27, 2006
Nephrology Dialysis Transplantation 2007 22(3):692-696; doi:10.1093/ndt/gfl686
This Article
Right arrow Extract Freely available
Right arrow FREE Full Text (PDF) Freely available
Right arrow All Versions of this Article:
22/3/692    most recent
gfl686v1
Right arrow Alert me when this article is cited
Right arrow Alert me if a correction is posted
Services
Right arrow Email this article to a friend
Right arrow Similar articles in this journal
Right arrow Similar articles in ISI Web of Science
Right arrow Similar articles in PubMed
Right arrow Alert me to new issues of the journal
Right arrow Add to My Personal Archive
Right arrow Download to citation manager
Right arrowRequest Permissions
Right arrow Disclaimer
Google Scholar
Right arrow Articles by Krumme, B.
Right arrow Articles by Hollenbeck, M.
Right arrow Search for Related Content
PubMed
Right arrow PubMed Citation
Right arrow Articles by Krumme, B.
Right arrow Articles by Hollenbeck, M.
Social Bookmarking
Add to CiteULike   Add to Connotea   Add to Del.icio.us  
What's this?

© The Author [2006]. Published by Oxford University Press on behalf of ERA-EDTA. All rights reserved. For Permissions, please email: journals.permissions@oxfordjournals.org

Doppler sonography in renal artery stenosis—does the Resistive Index predict the success of intervention?

Bernd Krumme1 and Markus Hollenbeck2

1Deutsche Klinik für Diagnostik, Division of Nephrology and Hypertension, Wiesbaden and 2Knappschaftskrankenhaus Bottrop, Division of Nephrology and Rheumatology, Bottrop, Germany

Correspondence and offprint requests to: Prof. Dr Bernd Krumme, Division of Nephrology and Hypertension, Deutsche Klinik für Diagnostik, Von Leyden-Str. 23, D-65191 Wiesbaden, Germany. Email: Krumme{at}nephrologie-wiesbaden.de

Keywords: colour Doppler ultrasound; Doppler sonography; ischaemic nephropathy; renal artery stenosis; renal ultrasound; renovascular disease



   Introduction
Top
 Introduction
Intrarenal Resistive Index and...
 Is the intrarenal Resistive...
 Conclusions
 References
 
Renal artery stenosis (RAS) may induce renovascular hypertension and ischaemic nephropathy. For decades, research has been focused on non-invasive diagnostic techniques, which might reliably predict the outcome of blood pressure and renal function after revascularization of RAS. In 1991, Geyskes and de Bruyn [1] found that captopril renography predicted the outcome of blood pressure in 94 patients with significant RAS with sensitivity and specificity of 91 and 62%, respectively. However, this technique shows less diagnostic accuracy in patients with renal failure [2]. Schoenberg et al. [3] have shown that magnetic resonance angiography is a reliable tool for the non-invasive grading of RAS, if phase-contrast flow measurement is achieved [3]. This technique offers important information on functional consequences of stenoses with potential impact on the glomerular filtration rate. Nevertheless, a correlation with the clinical outcome after intervention in patients with significant RAS is still not available.

Doppler sonography has been steadily improved over the last years and is now frequently used as first-line screening test for patients with suspected RAS [4–7]. In addition, arguments have been presented to indicate that it may also be useful to predict outcome after revascularization. The combined approach to the main renal artery, as well as to the intrarenal arteries, seems to be the ideal technique to overcome the limitations of this tool, such as impaired visualization due to bowel movement and obesity [5,6,8].

The ‘extra-renal’ parameters of choice are the peak systolic velocity, obtained in the main renal artery, as well as the renal aortic ratio of the maximum blood flow velocities, determined in the aorta and in the main renal artery. Significant RAS is present, if peak systolic velocity >1.8–2.0 m/s or renal aortic ratio >3.5 are obtained [4–8] (Figure 1).


Figure 1
View larger version (72K):
[in this window]
[in a new window]
[Download PowerPoint slide]
  		Fig. 1. The green colour indicates high blood flow velocities and turbulences near the ostium of the left renal artery scanned with the patient in a supine position. Peak systolic velocity of 269 cm/s detected with an angle of 53° indicates moderate renal artery stenosis.

 
Additional intrarenal scanning permits the diagnosis of RAS without direct imaging of the main renal artery. In 1994, Schwerk et al. [9] introduced the Resistive Index (RI) obtained in the interlobar arteries as a reliable indirect parameter for detecting RAS. The authors calculated the side-to-side difference of intrarenal RI >5% with the lower RI in the post-stenotic kidney. Sensitivity and specificity were 100 and 94%, respectively, for moderate and severe RAS [9]. In the meantime, intrarenal RI has been frequently evaluated for different nephrological issues [10,11]. In a single prospective study [12] a high intrarenal RI was found to be negatively correlated with the outcome of intervention in patients with atherosclerotic RAS. A high RI (RI ≥ 80) was felt to reflect advanced renal damage, which would explain the interventional treatment failure. However, these amazing results were not uniformly confirmed in different studies [13–15].

The aim of this review is to comment on the contradictory findings of recent papers and to shed some light on the mystification of intrarenal RI, with special attention paid to its use as a predictive parameter for the outcome of intervention in patients with RAS.



   Intrarenal Resistive Index and its affecting factors
Top
 Introduction
 Intrarenal Resistive Index and...
Is the intrarenal Resistive...
 Conclusions
 References
 
The RI is a ratio of peak systolic and end diastolic velocity, derived from the Doppler spectrum of any vessel (Figure 2). Initially this index was introduced by Pourcelot [16] for the grading of stenoses of the carotid artery. There is some evidence that several factors influence intrarenal RI: (i) the extent of stenosis; (ii) the distensibility/stiffness of the vascular system; (iii) non-renal factors and (iv) the location of intrarenal Doppler measurement.


Figure 2
View larger version (82K):
[in this window]
[in a new window]
[Download PowerPoint slide]
  		Fig. 2. Intrarenal RI is derived from the formula of Pourcelot [16]. RI of 51 is determined in the Doppler flow pattern of a kidney with proximal RAS. The ‘tardus-parvus’-flow pattern reveals low peak systolic and high end diastolic velocity resulting in low RI-values from 42 to 53.

 
Extent of stenosis
Significant narrowing of the vessel induces a reduction of the peak systolic flow velocity, including a loss of the so-called ‘early systolic peak’. While end diastolic velocity increases in stenoses, RI decreases, because PSV is calculated in the nominator of the ratio (Figure 2). The more severe the RAS, the lower the RI is determined [5].

Distensibility/stiffness of the arteries
In vitro experiments have shown that the degree of distensibility of the vessel has an important impact on the post-stenotic Doppler waveform. The loss of the early systolic peak is normal in an artery with high compliance; however, this is a sign of significant stenosis in an artery with low compliance. Therefore, a higher RI is measured in vessels with low compliance than in those with excellent compliance [17,18].

The interaction between distensibility and Doppler waveform of the vessel may explain the data of intrarenal RI, recently evaluated in patients with renal allografts [19,20]. Heine et al. [19] found a significant correlation between intrarenal RI, derived in 105 stable renal allografts, with parameters of atherosclerosis of the recipients, e.g. intima media thickness, Ankle Brachial Index and the Framingham risk score. Very recently we found corresponding data. Intrarenal RI of 76 renal allografts with stable renal function significantly correlated with the pulse wave velocity of the recipients, obtained from the carotid to the femoral artery [20].

In summary, the stiffness of the supplying arteries, e.g. the aorta or the iliac artery, have a significant impact on the RI derived in renal allografts. Both the in vitro data as well as those of transplanted grafts must be borne in mind when interpreting the RI of native kidneys. The Doppler signal of the kidney appears to be a mirror of the vascular system of the patient independently from the degree of renal damage. Consequently, there was no correlation found between RI and the glomerular filtration rate of the grafts in both trials [19,20]. In another study, correlation of RI with renal histopathological parameters revealed a relationship exclusively with the degree of renal arteriolosclerosis, measured as percentage of vessels showing wall thickening or hyaline change [21].

Non-renal factors
Further non-renal factors have an impact on the intrarenal RI of the kidneys. For example, tachycardia induces low values of RI, simply because the systolic peak begins earlier than in the case of normal heart rate. Similarly, bradycardia (heart rate <60 beats/min) induces high values of RI due to later beginning of the next systolic peak with less endiastolic velocity. Needless to say, the vascular resistance of kidney does not change with the heart rate. It is worth mentioning that in case of arrhythmias, RI does not give any information on renal perfusion. Especially in patients with atrial fibrillation, RI should not be used for the diagnosis of RAS.

In patients with insufficient aortic valve, high intrarenal RI is calculated due to the high amplitude of blood pressure. Vice versa, in patients with significant stenosis of the aortic valve, low RI is registered in the kidneys.

Acute swelling of the kidney leads to an increase in vascular resistance. Therefore, high RI is registered in patients with significant renal obstruction [22], with haemolytic uraemic syndrome [23], as well as in those with acute transplant rejection [24]. In these cases, renal Doppler sonography may be useful for therapeutic monitoring, rather than for making the final diagnosis.

The location of intrarenal Doppler measurement
Intrarenal RI decreases from the hilum of the kidney towards the renal cortex [18]. While the ‘early systolic peak’ frequently appears in the normal Doppler flow pattern of an hilar artery, this phenomenon is rarely detected in the interlobular renal arteries. Therefore, if intrarenal RI is calculated from the flow pattern of the hilar artery, higher values of RI are expected. This might be one reason for the discrepancy in current published data. However, it is common sense to calculate intrarenal RI without the ‘early systolic peak’ obtained from the spectra of the interlobar or segmental arteries.

Bearing all non-renal factors in mind, it might be valid to question whether high intrarenal RI is really an indicator of advanced morphological damage and thus helpful in predicting interventional outcome in patients with RAS?



   Is the intrarenal Resistive Index predictive for patients with RAS?
Top
 Introduction
 Intrarenal Resistive Index and...
 Is the intrarenal Resistive...
Conclusions
 References
 
Radermacher et al. [12] found that intrarenal RI ≥ 80 obtained in segmental renal arteries was highly predictive of treatment failure in patients with atherosclerotic RAS. In this single-centre prospective trial, 90 of 91 patients with RI < 80 showed improvement of blood pressure after angioplasty or stenting of RAS. Multivariate odds ratio of RI ≥ 80 for worsening of renal function was 100-fold higher than the odds ratio of other diagnostic tests or established predictive clinical parameters [12]. Due to this clear superiority in a single study, the Doppler parameter was implemented in several guidelines and reviews on the approach to patients with RAS [25,26]. However, there are essential limitations to the study. The authors did not clearly affirm whether they used the RI of the stenotic kidney or the RI of the contralateral side for statistical evaluation. This detail is important, due to the impact of stenotic grading on intrarenal RI. The lower the post-stenotic RI, the higher the percentage of luminal reduction of the renal artery [5]. Therefore it is useless to use post-stenotic RI to identify advanced renal damage. Because 47 patients with bilateral RAS were included in the study, post-stenotic RI was used for statistical evaluation in 36% of the patients [12]. It is likely that several of these patients with RI ≥ 80, who were treated with angioplasty, did not have severe RAS. In addition, it is notable that patients with a reduction in the diameter of renal arteries of at least 50%, which might be not significant, were included in the study [12]. This may explain the high rate of treatment failure in the group of patients with RI ≥ 80.

Recently, Voiculescu et al. [27] evaluated post-stenotic RI separately from contralateral RI in patients with unilateral RAS. The univariate odds ratio for contralateral RI ≥ 80 was not significant for the prediction of blood pressure outcome in this study. However, post-stenotic RI of <55, in combination with renin ratio of selective renal vein sampling, showed best sensitivity and specificity of 88 and 67%, respectively, for predicting blood pressure outcome after intervention [27]. It seems plausible that severe RAS detected by low post-stenotic RI (RI < 55) responds more frequently to intervention than moderate RAS with higher post-stenotic RI.

Although several recent studies did not explicitly calculate the predictive value of RI for the outcome of RAS after intervention, there are some important data worthy of mention.

In a huge group of 241 patients uniformly treated with stent angioplasty for severe RAS (≥70%), Zeller et al. [13] found, in 39 patients with RI > 80, significant improvement of blood pressure as well as improvement of renal function. Similarily, in a small study of 36 patients with successful revascularization of atherosclerotic renal artery stenosis, Garcia-Criado et al. [14] found no difference of renal function outcome between patients with intrarenal RI > 80 and those with RI < 80.

Soulez et al. [15] calculated the bilateral RI representing an average of RI measurements of both kidneys. A threshold of RI <75, together with a kidney length of >90 mm, predicted a favourable outcome after angioplasty with sensitivity and specificity of 81 and 50%, respectively. This low specificity does not really help the physician to decide for or against angioplasty for the patient.

Finally, the latter results confirm the early data of Frauchiger et al. [28], who studied the predictive value of the ratio of diastolic and systolic intrarenal flow in 32 patients with 35 interventions for RAS. They found that the ratio <0.30, corresponding to RI > 70, weakly correlated with clinical failure of subsequent renal artery intervention. However, in the majority of patients, a ratio >0.30, corresponding to normal RI, had no prognostic significance.



   Conclusions
Top
 Introduction
 Intrarenal Resistive Index and...
 Is the intrarenal Resistive...
 Conclusions
References
 
Many ‘non-renal’ factors affect the RI obtained in the intrarenal arteries of the kidney. These factors must be considered, if intrarenal RI is used as parameter to predict interventional success. The haemodynamic impact of the post-stenotic flow pattern in RAS prohibits the use of RI for the diagnosis of advanced renal damage in patients with severe RAS. The predictive value of RI in non-stenotic contralateral kidneys is contradictory in the recent literature. An RI ≥ 80 cannot be recommended as the predictive parameter of choice for the outcome of intervention in patients with significant unilateral RAS. However, low intrarenal post-stenotic RI indicates more severe stenosis, which is more likely to respond to intervention than low grade or moderate RAS. The current controversy must be solved by further studies.

Conflict of interest statement. None declered.



   References
Top
 Introduction
 Intrarenal Resistive Index and...
 Is the intrarenal Resistive...
 Conclusions
 References
 

  1. Geyskes GG and de Bruyn AJ. (1991) Captopril renography and the effect of percutaneous transluminal angioplasty on blood pressure in 94 patients with renal artery stenosis. Am J Hypertens 4:685S–689S.[Medline]
  2. Van Jaarsfeld BC, Krijnen P, Derckx FHM, Oei HY, Postma CT, Schalekamp MADH. (1997) The place of renal scintigraphy in the diagnosis of renal artery stenosis. Arch Intern Med 157:1226–1234.[Abstract]
  3. Schoenberg SO, Knopp MV, Londy F, et al. (2002) Morphologic and functional magnetic resonance imaging of renal artery stenosis: a multireader tricenter study. J Am Soc Nephrol 13:158–169.[Abstract/Free Full Text]
  4. Hoffmann U, Edwards JM, Carter S, et al. (1991) Role of duplex scanning for the detection of atherosclerotic renal artery disease. Kidney Int 39:1232–1239.[ISI][Medline]
  5. Krumme B, Blum U, Schwertfeger E, et al. (1996) Diagnosis of renovascular disease by intra- and extrarenal Doppler scanning. Kidney Int 50:1288–1292.[ISI][Medline]
  6. Radermacher J, Chavan A, Schaffer J, et al. (2000) Detection of significant renal artery stenosis with color Doppler sonography: combining extrarenal and intrarenal approaches to minimize technical failure. Clin Nephrol 53:333–343.[ISI][Medline]
  7. Bardelli M, Veglio F, Arosio E, et al. (2006) New intrarenal echo-Doppler velocimetric indices for the diagnosis of renal artery stenosis. Kidney Int 69:580–587.[CrossRef][ISI][Medline]
  8. Malatino LS, Polizzi G, Garozzo M, et al. (1998) Diagnosis of renovascular disease by extra- and intrarenal Doppler parameters. Angiology 49:707–721.[ISI][Medline]
  9. Schwerk WB, Restrepo IK, Stellwaag M, et al. (1994) Renal artery stenosis: grading with image-directed Doppler US evaluation of renal resistive index. Radiology 190:785–790.[Abstract/Free Full Text]
  10. Krumme B. (2006) Renal Doppler sonography – update in clinical nephrology. Nephron Clin Pract 103:c24–c28.[CrossRef][Medline]
  11. Pearce JD, Edwards MS, Craven TE, et al. (2005) Renal duplex parameters, blood pressure, and renal function in elderly people. Am J Kidney Dis 45:842–850.[CrossRef][ISI][Medline]
  12. Radermacher J, Chavan A, Bleck J, et al. (2001) Use of Doppler ultrasonography to predict the outcome of therapy for renal-artery stenosis. N Engl J Med 344:410–417.[Abstract/Free Full Text]
  13. Zeller T, Muller C, Frank U, et al. (2003) Stent angioplasty of severe atherosclerotic ostial renal artery stenosis in patients with diabetes mellitus and nephrosclerosis. Catheter Cardiovasc Intervent 58:510–515.[CrossRef][ISI][Medline]
  14. Garcia-Criado A, Gilabert R, Nicolau C, et al. (2005) Value of Doppler sonography for predicting clinical outcome after renal artery revascularization in atherosclerotic renal artery stenosis. J Ultrasound Med 24:1641–1647.[Abstract/Free Full Text]
  15. Soulez G, Therasse E, Qanadli SD, et al. (2003) Prediction of clinical response after renal angioplasty: respective value of renal Doppler sonography and scintigraphy. Am J Radiology 181:1029–1035.
  16. Pourcelot L. (1971) Applications cliniques de léxamen Doppler examinations transcutane. In Peronneau P (Ed.). Velocimetrie Ultrasonore Doppler(Inserm, Paris) pp. 213–217.
  17. Halpern EJ, Deane CR, Needleman L, Merton DA, East SA. (1995) Normal renal artery spectral Doppler waveform: a closer look. Radiology 196:667–673.[Abstract/Free Full Text]
  18. Bude RO, Rubin JM, Platt JF, Fechner KP, Adler RS. (1994) Pulsus tardus:its cause and potential limitations in detection of arterial stenosis. Radiology 190:779–784.[Abstract/Free Full Text]
  19. Heine GH, Gerhardt MK, Ulrich C, Köhler H, Girndt M. (2005) Renal Doppler resistance indices are associated with systemic atherosclerosis in kidney transplant recipients. Kidney Int 68:878–885.[CrossRef][ISI][Medline]
  20. Schwenger V, Keller T, Hofmann N, et al. (2006) Intrarenal color Doppler indices of renal allografts depend on vascular stiffness of the transplant recipients. Am J Transplant 6:2721–2724.[CrossRef][ISI][Medline]
  21. Ikee R, Kobayashi S, Hemmi N, et al. (2005) Correlation between the Resistive Index by Doppler ultrasound and kidney function and histology. Am J Kid Dis 46:603–609.[CrossRef][ISI][Medline]
  22. Opdenakker L, Oyen R, Vervloessem I. (1998) Acute obstruction of the renal collecting system: the intrarenal resistive index is a useful yet time-dependent parameter for diagnosis. Eur Radiol 8:1429–1432.[CrossRef][ISI][Medline]
  23. Patriquin H, O’Regan S, Robitaille P, Paltiel H. (1989) Hemolytic–uremic syndrome: intrarenal arterial Doppler patterns as a useful guide to therapy. Radiology 172:625–628.[Abstract/Free Full Text]
  24. Hollenbeck M, Hilbert N, Meusel F, Willers R, Grabensee B. (1994) Increasing sensitivity and specificity of Doppler sonographic detection of renal transplant rejection with serial investigation technique. Clin Investig 72:609–615.[ISI][Medline]
  25. Rundback JH, Sacks D, Kent C, et al. (2002) Guidelines for the reporting of renal artery revascularization in clinical trials. J Vasc Interv Radiol 13:959–974.[ISI][Medline]
  26. Chonchol M and Linas S. (2006) Diagnosis and management of ischaemic nephropathy. Clin J Am Soc Nephrol 1:172–181.
  27. Voiculescu A, Schmitz M, Plum J, et al. (2006) Duplex ultrasound and rennin ratio predict treatment failure after revascularization for renal artery stenosis. Am J Hypertens 19:756–763.[CrossRef][ISI][Medline]
  28. Frauchiger B, Zierler R, Bergelin RO, Isaacson JA, Strandness DE, Jr. (1996) Prognostic significance of intrarenal resistance indices in patients with renal artery interventions: a preliminary duplex sonographic study. Cardiovascular Surg 4:324–330.
Received for publication: 4. 9.06
Accepted in revised form: 24.10.06


Add to CiteULike CiteULike   Add to Connotea Connotea   Add to Del.icio.us Del.icio.us    What's this?


This article has been cited by other articles:


Home page
 Am. J. Roentgenol.Home page
K. B. Taori, R. S. Chaudhary, V. Attarde, S. Dhakate, V. Sheorain, P. Nimbalkar, and P. N. Wasnik
Renal Doppler Indices in Sickle Cell Disease: Early Radiologic Predictors of Renovascular Changes
Am. J. Roentgenol., July 1, 2008; 191(1): 239 - 242.
[Abstract] [Full Text] [PDF]

This Article
Right arrow Extract Freely available
Right arrow FREE Full Text (PDF) Freely available
Right arrow All Versions of this Article:
22/3/692    most recent
gfl686v1
Right arrow Alert me when this article is cited
Right arrow Alert me if a correction is posted
Services
Right arrow Email this article to a friend
Right arrow Similar articles in this journal
Right arrow Similar articles in ISI Web of Science
Right arrow Similar articles in PubMed
Right arrow Alert me to new issues of the journal
Right arrow Add to My Personal Archive
Right arrow Download to citation manager
Right arrowRequest Permissions
Right arrow Disclaimer
Google Scholar
Right arrow Articles by Krumme, B.
Right arrow Articles by Hollenbeck, M.
Right arrow Search for Related Content
PubMed
Right arrow PubMed Citation
Right arrow Articles by Krumme, B.
Right arrow Articles by Hollenbeck, M.
Social Bookmarking
Add to CiteULike   Add to Connotea   Add to Del.icio.us  
What's this?