Добавил:
Sekretar
kiopkiopkiop18@yandex.ru
t.me/Prokururor I Вовсе не секретарь, но почту проверяю
Опубликованный материал нарушает ваши авторские права? Сообщите нам.
Вуз:
Предмет:
Файл:Ординатура / Хирургия / Библиотека им академика М.И. Перельмана / Книга_3608_Библиотеки_им_академика_М_И_Перельмана
.pdf
fibrosis (NSF), an exceedingly rare condition that involves fibrosis
BC
of the skin, joints, eyes, and internal organs.
93–95
Current recommendations advise against administering gadolinium contrast
to individuals with a GFR below 30 mL/min/1.73m2 or those with
acute renal failure or acute deterioration of chronic renal failure.
95
COMPUTED TOMOGRAPHIC ANGIOGRAPHY
Computed tomographic angiography (also see Chapter 14) can
be performed rapidly and safely for assessment of renal artery disease. Multidetector-row CTA provides excellent image quality with
higher resolution than could be obtained previously with singledetector-row technology. Most clinical imaging centers currently
use 64- to 256-multidetector-row scanners, with 320-multidetector-row scanners currently reserved mostly for research applications or for studying the coronary arteries and bypass grafts.
Advantages of CTA over catheter-based angiography are
98–103
96,97
: volumetric acquisition, demonstrating better visualization of the anatomy from multiple angles and in multiple planes after a single
acquisition; improved visualization of soft tissues and other adjacent anatomical structures; less invasive and thus fewer complications; and lower cost.
Computed tomographic angiography has several advantages
over MRA, such as higher spatial and temporal resolution, absence
of flow-related phenomena that may distort MRA images, and capability to visualize calcification and metallic implants such as endovascular stents or stent grafts. Computed tomographic angiography
also involves markedly decreased total examination time, with
most 64-multidetector scanners currently performing a complete
vascular examination of the abdominal aorta, mesenteric, renal,
and iliac arteries in 5 to 10 seconds with submillimeter spatial
resolution. When exposure to ionizing radiation is a concern (e.g.,
in younger patients), MRA may be the preferred imaging modality.
The increased speed of acquisitions coupled with subsecond
gantry rotations obtained with multidetector-row CTA allows for
greater longitudinal coverage for a given scan duration and greater
spatial resolution.
104
This may not be of as much importance for
assessing renal artery disease, but it has great advantages when
assessing the thoracoabdominal, aortoiliac, and lower-extremity
inflow and runoff, which may require up to 1400 mm of coverage.
105
Rapid acquisition of images allows for reduction in the amount
of iodinated contrast material needed while maintaining excellent
and uniform vascular enhancement.
98,101–103,106
Thin beam collimation (<1 mm), rotational speed of the tube, and
rate of table feed are key parameters in determining imaging protocols. The first set of images produced are sequential or overlapping
axial images, which should be interpreted with full attention to all
nonvascular structures including bones, bowel, visceral organs, and
lung. To create angiographic representations, post-processing
of the volumetric data is necessary. The best post-processed
images are created from overlapping submillimeter reconstructed
images (
Fig. 23-8). In the absence of overlap, the angiographic
images may have a marked stair-step appearance.
Over the past several years, more complex post-processing algorithms have been formulated to display volumetric data, including maximum intensity projection (MIP), shaded surface display
(SSD), and volumetric rendering (VR).
106–108
These techniques allow
manipulation of raw data so as to optimize visualization of relevant lesions or disease processes. An important common pitfall is
selective visualization of the maximally opacified vascular lumen.
Both automated and manual creation of post-processed images
risk inadvertent rejection of critical vascular and nonvascular
information. Post-processed images alone should never be used for
interpretation of CT angiography.
The sensitivity of CTA for RAS ranges from 89% to 100% and
specificity from 82% to 100%
105
77,103,105,109–113
(Table 23-6). The area
of acquisition should include the area from just proximal to the
celiac artery to and including the iliac arteries. This will ensure
that accessory renal arteries are detected and associated aortic
and visceral artery pathology is not overlooked.
Results obtained using duplex ultrasound, MRA, or CTA are not
nearly as good for assessing RAS secondary to FMD; catheter-based
angiography remains the imaging modality of choice if FMD is
suspected.
6,114
CATHETER-BASED ANGIOGRAPHY
Although duplex ultrasonography, MRA, and CTA have replaced
catheter-based angiography for the diagnosis of RAS in most circumstances, catheter-based angiography remains the gold standard. It is the most accurate test to diagnose RAS secondary to both
atherosclerosis and FMD. It can clearly visualize branch vessels and
cortical blood flow and is excellent for identifying accessory renal
arteries.
Digital subtraction angiography (DSA) has replaced screenfilm angiography in the majority of institutions for vascular applications. The resolution of DSA is less than that of screen film but
can approach three to four line pairs per millimeter with current
equipment (see
Fig. 23-1). The standard imaging matrix is now
1024 × 1024, with image intensifiers that range up to 16 inches in
diameter. Flat-panel image intensifiers will soon become available.
It is important to recognize that the renal arteries often come off
303
CH
23
CLINICAL EVALUATION OF RENAL ARTERY DISEASE
A
FIGURE 238 Three-dimensional (3D) computed tomographic angiogram (CTA) of renal arteries with 250 multidetector CT scanner. Volume rendering
(A) and maximal intensity projection (MIP) (B-C) demonstrating a dissection and severe focal stenosis of right renal artery and a normal left renal artery.
304
Данная книга находится в списке для перевода на русский язык сайта https://meduniver.com/
Accuracy of Computed Tomographic
TABLE 23-6
AUTHOR
CH
23
Kaatee
111
Kim
Johnson
Qanadli
112
113
110
Willmann
Vasbinder
128
Eklof
82
Rountas
of the aorta posteriorly, and therefore oblique views of the aorta
may be needed to adequately visualize the origin of the renal
arteries. Pressure gradients should also be obtained to confirm the
physiological significance of a given lesion.
New developments in hardware and software have led to
greater diagnostic accuracy and better safety. Bolus chasing, rapid
image acquisition, vessel diameter analysis, regional pixel shifting,
image stacking, 3D reconstructions from rotational angiograms,
and angioscopic representations of DSA data are now routinely
available from manufacturers.
Carbon dioxide (CO2) angiography provides an alternative to
conventional angiography or DSA using iodinated contrast agents.
This may be particularly useful in patients with renal insufficiency
in whom contrast exposure may accelerate the decline of renal
function. When compared to conventional angiography, CO
ography has a sensitivity of 83% and a specificity of 99%.
Advantages of DSA are the high resolution compared to current
cross-sectional imaging techniques, ability to selectively evaluate
individual vessels, access direct physiological information such
as pressure gradients, and utilization as a platform for intervention.
Disadvantages are exposure to ionizing radiation, use of iodinated contrast agents (contrast-induced nephropathy), and risks
related to vascular access (pseudoaneurysm, hematoma, retroperitoneal bleed) and catheterization (atheromatous embolization).
Nevertheless, until an alternative platform is developed for intervention or completely MR-compatible devices become available,
DSA will continue to have a central role in the management of
patients with vascular disease.
RENAL ANGIOGRAPHY AT THE TIME OF CARDIAC
CATHETERIZATION
This controversial subject has led to numerous debates over the
most appropriate management strategy for patients with CAD and
possible RAS. It has been demonstrated that patients with CAD
have a higher prevalence of RAS than the general population. In
addition, patients with RAS have a markedly increased mortality
from cardiovascular disease. Conlon et al. reported that the 4-year
survival for patients with no RAS detected at the time of cardiac
catheterization was 90% compared to survival rates of 70% for 50%
to 75% stenosis, 68% for 75% to 95% stenosis, and 48% for more than
95% stenosis.
eterization state that the procedure can be performed accurately
with no added risk and provide the cardiologist with knowledge
that the patient has RAS so that the patient can then be followed
serially and treated with optimal secondary preventive measures.
Those against routine angiography claim that knowing that the
patient has RAS adds nothing to the patient's overall management
other than to tempt the angiographer to stent the stenotic lesion
in the absence of accepted clinical indications.
termed the renal oculosten(t)otic reflex.
Angiography for Assessment of Visceral and
Renal Artery Stenosis
YEAR PATIENTS
1997 71 92-100 96-100
1998 50 90-100 97
1999 25 89-94 87-99
2000 47 91 100
109
2003 46 91-92 99
130
2004 402 64 92
2005 58 94 62
2007 58 94 93
30,122
Proponents of angiography at the time of cath-
SENSITIVITY
%
105,115–119
124
SPECIFICITY
46,123
This has been
%
120,121
angi-
2
It is appropriate to perform renal angiography at the time of
cardiac catheterization if acceptable indications for renal artery
intervention are present.
125
Further prospective natural history
studies in this asymptomatic population are needed, however,
to answer the question of whether routine screening should be
performed at the time of cardiac catheterization.
REFERENCES
1. Pleis JR, Lucas JW, Ward BW: Summary health statistics for U.S. adults: National Health
Interview Survey, 2008, Vital Health Stat 10(242):1–157, 2009.
2. Olin JW, Melia M, Young JR, et al: Prevalence of atherosclerotic renal artery stenosis in
patients with atherosclerosis elsewhere, Am J Med 88(1N):46N–51N, 1990.
3. Harding MB, Smith LR, Himmelstein SI, et al: Renal artery stenosis: prevalence and
associated risk factors in patients undergoing routine cardiac catheterization, J Am Soc
Nephrol 2(11):1608–1616, 1992.
4. Safian RD, Textor SC: Renal-artery stenosis, N Engl J Med 344(6):431–442, 2001.
5. Dworkin LD, Cooper CJ: Clinical practice. Renal-artery stenosis, N Engl J Med 361(20):
1972–1978, 2009.
6. Olin JW, Sealove BA: Diagnosis, management, and future developments of fibromuscular
dysplasia, J Vasc Surg 53(3):826–836, 2011.
7. Olin JW: Atherosclerotic renal artery disease, Cardiol Clin 20(4):547–562, 2002.
8. Connolly JO, Higgins RM, Walters HL, et al: Presentation, clinical features and outcome in
different patterns of atherosclerotic renovascular disease, QJM 87(7):413–421, 1994.
9. Mailloux LU, Napolitano B, Bellucci AG, et al: Renal vascular disease causing end-stage
renal disease, incidence, clinical correlates, and outcomes: a 20-year clinical experience,
Am J Kidney Dis 24(4):622–629, 1994.
10. Mailloux LU, Bellucci AG, Napolitano B, et al: Survival estimates for 683 patients starting
dialysis from 1970 through 1989: identification of risk factors for survival, Clin Nephrol
42(2):127–135, 1994.
11. de Mast Q, Beutler JJ: The prevalence of atherosclerotic renal artery stenosis in risk groups:
a systematic literature review, J Hypertens 27(7):1333–1340, 2009.
12. Hansen KJ, Edwards MS, Craven TE, et al: Prevalence of renovascular disease in the elderly:
a population-based study, J Vasc Surg 36(3):443–451, 2002.
13. Dustan HP, Humphries AW, DeWolfe VG: Normal arterial pressure in patients with renal
arterial stenosis, JAMA 187:1028–1029, 1964.
14. Davis BA, Crook JE, Vestas RE, et al: Prevalence of renovascular hypertension in patients
with grade III or IV hypertensive retinopathy, N Engl J Med 301:1273–1276, 1979.
15. Chobanian AV, Bakris GL, Black HR, et al: The Seventh Report of the Joint National
Committee on Prevention, Detection, Evaluation, and Treatment of High Blood Pressure:
the JNC 7 Report, JAMA 289(19):2560–2571, 2003.
16. Gifford RW Jr, McCormack LJ, Poutasse EF: The atrophic kidney: its role in hypertension,
Mayo Clin Proc 40(834):852, 1965.
17. Lawrie GM, Morris GC Jr, Glaeser DH, et al: Renovascular reconstruction: factors
affecting long-term prognosis in 919 patients followed up to 31 years, Am J Cardiol
63(15):1085–1092, 1989.
18. Textor SC, Tarazi RC, Novick AC, et al: Regulation of renal hemodynamics and glomerular
filtration in patients with renovascular hypertension during converting enzyme inhibition
with captopril, Am J Med 76(5B):29–37, 1984.
19. Textor SC, Novick AC, Steinmuller DR, et al: Renal failure limiting antihypertensive therapy as
an indication for renal revascularization. A case report, Arch Intern Med 143(11):2208–2211,
1983.
20. Silas JH, Klenka Z, S olomon SA, et al: Captopril induced reversible renal failure: a marker of
renal artery stenosis affecting a solitary kidney, BMJ 286(6379):1702–1703, 1983.
21. Packer M, Lee WH, Medina N, et al: Functional renal insufficiency during long-term therapy
with captopril and enalapril in severe chronic heart failure, Ann Intern Med 106:346–354,
1987.
22. Textor SC: Renal failure related to ACE inhibitors, Semin Nephrol 17:67–76, 1997.
23. Scoble JE, Maher ER, Hamilton G: Atherosclerotic renovascular disease causing renal
impairment–a case for treatment, Clin Nephrol 31:119–122, 1989.
24. Scoble JE: Renal artery stenosis as a cause of renal impairment: implications for treatment
of hypertension and congestive heart failure, J R Soc Med 92(10):505–510, 1999.
25. Gray BH, Olin JW, Childs MB, et al: Clinical benefit of renal artery angioplasty with stenting for
the control of recurrent and refractory congestive heart failure, Vasc Med 7(4):275–279, 2002.
26. Pickering TG, Herman L, Devereux RB, et al: Recurrent pulmonary oedema in hyper-
tension due to bilateral renal artery stenosis: treatment by angioplasty or surgical revascularisation, Lancet 2(8610):551–552, 1988.
27. Diamond JR: Flash pulmonary edema and the diagnostic suspicion of occult renal artery
stenosis, Am J Kidney Dis 21(3):328–330, 1993.
28. Khosla S, Kunjummen B, Manda R, et al: Prevalence of renal artery stenosis requiring
revascularization in patients initially referred for coronary angiography, Catheter
Cardiovasc Interv 58(3):400–403, 2003.
29. Scobel JE: The epidemiology and clinical presentation of atherosclerotic renal artery
disease. In Novick AC, Scoble JE, Halmilton G, editors: Renal vascular disease, London,
1996, WB Saunders Co, Ltd, pp 303–314.
30. Conlon PJ, Little MA, Pieper K, et al: Severity of renal vascular disease predicts mortality in
patients undergoing coronary angiography, Kidney Int 60(4):1490–1497, 2001.
31. Rihal CS, Textor SC, Breen JF, et al: Incidental renal artery stenosis among a prospective
31
cohort of hypertensive patients undergoing coronary angiography, Mayo Clin Proc
77(4):309–316, 2002.
32. Weber-Mzell D, Kotanko P, Schumacher M, et al: Coronary anatomy predicts presence
or absence of renal artery stenosis. A prospective study in patients undergoing cardiac
catheterization for suspected coronary artery disease, Eur Heart J 23(21):1684–1691, 2002.
33. Louie J, Isaacson JA, Zierler RE, et al: Prevalence of carotid and lower extremity arterial
disease in patients with renal artery stenosis, Am J Hypertens 7(5):436–439, 1994.
34. Conlon P, O'Riordan E, Kalra P: New insights into the epidemiologic and clinical
manifestations of atherosclerotic renovascular disease, Am J Kidney Dis 35(4):573–587, 2000.
35. Dorros G, Jaff M, Mathiak L, et al: Four-year follow-up of Palmaz-Schatz stent
revasculariza tion as treatment for atherosclerotic renal artery stenosis, Circulation 98(7):
642–647, 1998.
36. Eipper DF, Gifford RW Jr, Stewart B, et al: Abdominal bruits in renovascular hypertension,
Am J Cardiol 37:48–52, 1976.
37. Olin JW: Evaluation of the peripheral circulation. In Izzo JL, Sicca DA, Black HR, editors:
Hypertension primer, ed 4, Dallas, 2007, American Heart Association, pp 374–378.
38. Canzanello VJ, Textor SC: Noninvasive diagnosis of renovascular disease, Mayo Clin Proc
69(12):1172–1181, 1994.
39. Emovon OE, Klotman PE, Dunnick NR, et al: Renovascular hypertension in blacks, Am
J Hypertens 9(1):18–23, 1996.
40. Maxwell MH, Lupu AN, Taplin GV: Radioisotope renogram in renal arterial hypertension, J
Urol 100(4):376–383, 1968.
41. Ploth DW: Angiotensin-dependent renal mechanisms in two-kidney, one-clip renal
vascular hypertension, Am J Physiol 245(2):F131–F141, 1983.
42. Nally JV, Barton DP: Contemporary approach to diagnosis and evaluation of renovascular
hypertension, Urol Clin North Am 28(4):781–791, 2001.
43. Black HR, Bourgoignie JJ, Pickering T, et al: Report of the Working Party Group for Patient
Selection and Preparation, Am J Hypertens 4(12 Pt 2):745S–746S, 1991.
44. Setaro JF, Chen CC, Hoffer PB, et al: Captopril renography in the diagnosis of renal artery
stenosis and the prediction of improvement with revascularization. The Yale Vascular
Center experience, Am J Hypertens 4(12 Pt 2):698S–705S, 1991.
45. Setaro JF, Saddler MC, Chen CC, et al: Simplified captopril renography in diagnosis and
treatment of renal artery stenosis, Hypertension 18(3):289–298, 1991.
46. Olin JW, Begelman SM: Renal artery disease. In Topol E, editor: Textbook of Cardiovascular
medicine, ed 2, Philadelphia, 2002, Lippincott Raven, pp 2139–2159.
47. Fommei E, Ghione S, Hilson AJ, et al: Captopril radionuclide test in renovascular
hypertension: a European multicentre study. European Multicentre Study Group, Eur J
Nucl Med 20(7):617–623, 1993.
48. Carman TL, Olin JW: Diagnosis of renal artery stenosis: what is the optimal diagnostic test?
Curr Interv Cardiol Rep 2(2):111–118, 2000.
49. Hansen KJ, Tribble RW, Reavis SW, et al: Renal duplex sonography: evaluation of clinical
utility, J Vasc Surg 12(3):227–236, 1990.
50. Hoffmann U, Edwards JM, Carter S, et al: Role of duplex scanning for the detection of
atherosclerotic renal artery disease, Kidney Int 39(6):1232–1239, 1991.
51. Kohler TR, Zierler RE, Martin RL, et al: Noninvasive diagnosis of renal artery stenosis by
ultrasonic duplex scanning, J Vasc Surg 4(5):450–456, 1986.
52. Malatino LS, Polizzi G, Garozzo M, et al: Diagnosis of renovascular disease by extra- and
intrarenal Doppler parameters, Angiology 49(9):707–721, 1998.
53. Miralles M, Cairols M, Cotillas J, et al: Value of Doppler parameters in the diagnosis of renal
artery stenosis, J Vasc Surg 23(3):428–435, 1996.
54. Olin JW: Role of duplex ultrasonography in screening for significant renal artery disease,
Urol Clin North Am 21(2):215–226, 1994.
55. Williams GJ, Macaskill P, Chan SF, et al: Comparative accuracy of renal duplex sonographic
parameters in the diagnosis of renal artery stenosis: paired and unpaired analysis, AJR Am
J Roentgenol 188(3):798–811, 2007.
56. Olin JW, Piedmonte MR, Young JR, et al: The utility of duplex ultrasound scanning of the renal
arteries for diagnosing significant renal artery stenosis, Ann Intern Med 122(11):833–838, 1995.
57. Carman TL, Olin JW, Czum J: Noninvasive imaging of the renal arteries, Urol Clin North Am
28(4):815–826, 2001.
58. Radermacher J, Chavan A, Bleck J, et al: Use of Doppler ultrasonography to predict the
outcome of therapy for renal-artery stenosis, N Engl J Med 344(6):410–417, 2001.
59. Soulez G, Therasse E, Qanadli SD, et al: Prediction of clinical response after renal
angioplasty: respective value of renal Doppler sonography and scintigraphy, AJR Am J
Roentgenol 181(4):1029–1035, 2003.
60. Crutchley TA, Pearce JD, Craven TE, et al: Clinical utility of the resistive index in atherosclerotic renovascular disease, J Vasc Surg 49(1):148–155, 2009 .
61. Zeller T, Muller C, Frank U, et al: Stent angioplasty of severe atherosclerotic ostial renal
artery stenosis in patients with diabetes mellitus and nephrosclerosis, Catheter Cardiovasc
Interv 58(4):510–515, 2003.
62. Zeller T, Frank U, Muller C, et al: Predictors of improved renal function after percutaneous
stent-supported angioplasty of severe atherosclerotic ostial renal artery stenosis,
Circulation 108(18):2244–2249, 2003.
63. Hirsch AT, Haskal ZJ, Hertzer NR, et al: ACC/AHA 2005 guidelines for the management of
patients with peripheral arterial disease (lower extremity, renal, mesenteric, and abdominal
aortic): executive summary a collaborative report from the American Association for
Vascular Surgery/Society for Vascular Surgery, Society for Cardiovascular Angiography and
Interventions, Society for Vascular Medicine and Biology, Society of Interventional Radiology,
and the ACC/AHA Task Force on Practice Guidelines (Writing Committee to Develop
Guidelines for the Management of Patients With Peripheral Arterial Disease) endorsed by the
American Association of Cardiovascular and Pulmonary Rehabilitation; National Heart, Lung,
and Blood Institute; Society for Vascular Nursing; TransAtlantic Inter-Society Consensus; and
Vascular Disease Foundation, J Am Coll Cardiol 47(6):1239–1312, 2006.
64. Taylor DC, Moneta GL, Strandness DE Jr: Follow-up of renal artery stenosis by duplex
ultrasound, J Vasc Surg 9(3):410–415, 1989.
65. Hudspeth DA, Hansen KJ, Reavis SW, et al: Renal duplex sonography after treatment of
renovascular disease, J Vasc Surg 18(3):381–388, 1993.
66. Bakker J, Beutler JJ, Elgersma OE, et al: Duplex ultrasonography in assessing restenosis of
renal artery stents, Cardiovasc Intervent Radiol 22:475–480, 1999.
67. G alin I, Trost B, Kang K, et al: Validation of renal duplex ultrasound in detecting renal artery
stenosis post stenting, J Am Coll Cardiol 51(Suppl I) (10):A317, 2008.
68. White CJ, Olin JW: Diagnosis and management of atherosclerotic renal artery stenosis:
improving patient selection and outcomes, Nat Clin Pract Cardiovasc Med 6(3):176–190, 2009.
69. Soulez G, Oliva VL, Turpin S, et al: Imaging of renovascular hypertension: respective
values of renal scintigraphy, renal Doppler US, and MR angiography, Radiographics
20(5):1355–1368, 2000.
70. Schoenberg SO, Knopp MV, Londy F, et al: Morphologic and functional magnetic
resonance imaging of renal artery stenosis: a multireader tricenter study, J Am Soc Nephrol
13(1):158–169, 2002.
71. Aumann S, Schoenberg SO, Just A, et al: Quantification of renal perfusion using an
intravascular contrast agent (part 1): results in a canine model, Magn Reson Med 49(2):
276–287, 2003.
72. Bakker J, Beek FJ, Beutler JJ, et al: Renal artery stenosis and accessory renal arteries:
accuracy of detection and visualization with gadolinium-enhanced breath-hold MR
angiography, Radiology 207(2):497–504, 1998.
73. Schoenberg SO, Essig M, Bock M, et al: Comprehensive MR evaluation of renovascular
disease in five breath holds, J Magn Reson Imaging 10(3):347–356, 1999.
74. Hahn U, Miller S, Nagele T, et al: Renal MR angiography at 1.0 T: three-dimensional (3D)
phase-contrast techniques versus gadolinium-enhanced 3D fast low-angle shot breathhold imaging, AJR Am J Roentgenol 172(6):1501–1508, 1999.
75. Tan KT, van Beek EJ, Brown PW, et al: Magnetic resonance angiography for the diagnosis
of renal artery stenosis: a meta-analysis, Clin Radiol 57(7):617–624, 2002.
76. De Cobelli F, Vanzulli A, Sironi S, et al: Renal artery stenosis: evaluation with breath-hold,
three-dimensional, dynamic, gadolinium-enhanced versus three-dimensional, phasecontrast MR angiography, Radiology 205(3):689–695, 1997.
77. Fain SB, King BF, Breen JF, et al: High-spatial-resolution contrast-enhanced MR angiography of the renal arteries: a prospective comparison with digital subtraction
angiography, Radiology 218(2):481–490, 2001.
78. Hany TF, Debatin JF, Leung DA, et al: Evaluation of the aortoiliac and renal arteries:
comparison of breath-hold, contrast-enhanced, three-dimensional MR angiography with
conventional catheter angiography, Radiology 204(2):357–362, 1997.
79. Rieumont MJ, Kaufman JA, G eller SC, et al: Evaluation of renal artery stenosis with dynamic
gadolinium-enhanced MR angiography, AJR Am J Roentgenol 169(1):39–44, 1997.
80. Snidow JJ, Johnson MS, Harris VJ, et al: Three-dimensional gadolinium-enhanced MR
angiography for aortoiliac inflow assessment plus renal artery screening in a single breath
hold, Radiology 198(3):725–732, 1996.
81. Bicakci K, Soker G, Binokay F, et al: Estimation of the ratio of renal artery stenosis with
magnetic resonance angiography using parallel imaging technique in suspected
renovascular hypertension, Nephron Clin Pract 104(4):c169–c175, 2006.
82. Rountas C, Vlychou M, Vassiou K, et al: Imaging modalities for renal artery stenosis in
suspected renovascular hypertension: prospective intraindividual comparison of color
Doppler US, CT angiography, GD-enhanced MR angiography, and digital subtraction
angiography, Ren Fail 29(3):295–302, 2007.
83. Stacul F, Gava S, Belgrano M, et al: Renal artery stenosis: comparative evaluation of
gadolinium-enhanced MRA and DSA, Radiol Med 113(4):529–546, 2008.
84. Glockner JF, Takahashi N, Kawashima A, et al: Non-contrast renal artery MRA using
an inflow inversion recovery steady state free precession technique (Inhance):
comparison with 3D contrast-enhanced MRA, J Magn Reson Imaging 31(6):1411–1418,
2010.
85. Korpraphong P, Tovanabutra P, Muangsomboon K: Renal artery stenosis: diagnostic
performance of balanced fast field gradient echo MRA, J Med Assoc Thai 92(8):1077–1083,
2009.
86. Maki JH, Wilson GJ, Eubank WB, et al: Navigator-gated MR angiography of the renal
arteries: a potential screening tool for renal artery stenosis, AJR Am J Roentgenol
188(6):W540–W546, 2007.
87. Utsunomiya D, Miyazaki M, Nomitsu Y, et al: Clinical role of non-contrast magnetic
resonance angiography for evaluation of renal artery stenosis, Circ J 72(10):1627–1630,
2008.
88. Wyttenbach R, Braghetti A, Wyss M, et al: Renal artery assessment with nonenhanced
steady-state free precession versus contrast-enhanced MR angiography, Radiology
245(1):186–195, 2007.
89. Prince MR, Chenevert TL, Foo TK, et al: Contrast-enhanced abdominal MR angiography:
optimization of imaging delay time by automating the detection of contrast material
arrival in the aorta, Radiology 203(1):109–114, 1997.
90. Zhang J, Pedrosa I, Rofsky NM: MR techniques for renal imaging, Radiol Clin North Am
41(5):877–907, 2003.
91. Saloner D: Determinants of image appearance in contrast-enhanced magnetic resonance
angiography: a review, Invest Radiol 33:488–495, 1998.
92. Thornton J, O'Callaghan J, Walshe J, et al: Comparison of digital subtraction angiography
with gadolinium-enhanced magnetic resonance angiography in the diagnosis of renal
artery stenosis, Eur Radiol 9(5):930–934, 1999.
93. Kribben A, Witzke O, Hillen U, et al: Nephrogenic systemic fibrosis: pathogenesis,
diagnosis, and therapy, J Am Coll Cardiol 53(18):1621–1628, 2009.
94. Perazella MA: Advanced kidney disease, gadolinium and nephrogenic systemic fibrosis:
the perfect storm, Curr Opin Nephrol Hypertens 18(6):519–525, 2009.
95. Prince MR, Zhang HL, Roditi GH, et al: Risk factors for NSF: a literature review, J Magn Reson
Imaging 30(6):1298–1308, 2009.
96. de Graaf FR, van Velzen JE, Witkowska AJ, et al: Diagnostic performance of 320-slice
multidetector computed tomography coronary angiography in patients after coronary
artery bypass grafting, Eur Radiol 21(11):2285–2296, 2011.
97. van Velzen JE, de Graaf FR, Kroft LJ, et al: Performance and efficacy of 320-row computed
tomography coronary angiography in patients presenting with acute chest pain: results
from a clinical registry, Int J Cardiovasc Imaging 2011. May 26. [Epub ahead of print] DOI
10.1007/s10554-011-9889-z
98. Rubin GD: Three-dimensional helical CT angiography, Radiographics 14(4):905–912, 1994.
99. Rubin GD: MDCT imaging of the aorta and peripheral vessels, Eur J Radiol 45(Suppl
1):S42–S49, 2003.
100. Rubin GD: 3-D imaging with MDC T, Eur J Radiol 45(Suppl 1):S37–S41, 2003.
101. Rubin GD: Techniques for performing multidetector-row computed tomographic
angiography, Tech Vasc Interv Radiol 4(1):2–14, 2001.
102. Bluemke DA, Chambers TP: Spiral CT angiography: an alternative to conventional
angiography, Radiology 195(2):317–319, 1995.
103. Liu PS, Platt JF: CT angiography of the renal circulation, Radiol Clin North Am 48(2):347–365,
2010.
305
CH
23
CLINICAL EVALUATION OF RENAL ARTERY DISEASE
306
Данная книга находится в списке для перевода на русский язык сайта https://meduniver.com/
104. Bluemke DA, Soyer PA, Chan BW, et al: Spiral CT during arterial portography: technique
and applications, Radiographics 15(3):623–637, 1995.
105. Olin JW, Kaufman JA, Bluemke DA, et al: Atherosclerotic Vascular Disease Conference.
American Heart Association, Imaging, Writing Group IV, Circulation 109:2626–2633,
2004.
106. Zeman RK, Silverman PM, Vieco PT, et al: CT angiography, AJR Am J Roentgenol
165(5):1079–1088, 1995.
107. Ibukuro K, Charnsangavej C, Chasen MH, et al: Helical CT angiography with multiplanar
CH
23
reformation: techniques and clinical applications, Radiographics 15(3):671–682, 1995.
108. Addis KA, Hopper KD, Iyriboz TA, et al: CT angiography: in vitro comparison of five
reconstruction methods, AJR Am J Roentgenol 177(5):1171–1176, 2001.
109. Willmann JK, Wildermuth S, Pfammatter T, et al: Aortoiliac and renal arteries: prospective
intraindividual comparison of contrast-enhanced three-dimensional MR angiography
and multi-detector row CT angiography, Radiology 226(3):798–811, 2003.
110. Qanadli SD, Mesurolle B, Coggia M, et al: Abdominal aortic aneurysm: pretherapy assessment
with dual-slice helical CT angiography, AJR Am J Roentgenol 174(1):181–187, 2000.
111. Kim TS, Chung JW, Park JH, et al: Renal artery evaluation: comparison of spiral CT
angiography to intra-arterial DSA, J Vasc Interv Radiol 9(4):553–559, 1998.
112. Kaatee R, Beek FJ, de Lange EE, et al: Renal artery stenosis: detection and quantification
with spiral CT angiography versus optimized digital subtraction angiography, Radiology
205(1):121–127, 1997.
113. Johnson PT, Halpern EJ, Kuszyk BS, et al: Renal artery stenosis: CT angiography–comparison
of real-time volume-rendering and maximum intensity projection algorithms, Radiology
211(2):337–343, 1999.
114. Slovut DP, Olin JW: Fibromuscular dysplasia, N Engl J Med 350(18):1862–1871, 2004.
115. Bosanac Z, Miller RJ, Jain M: Rotational digital subtraction carotid angiography: technique
and comparison with static digital subtraction angiography, Clin Radiol 53(9):682–687, 1998.
116. Seymour HR, Matson MB, Belli AM, et al: Rotational digital subtraction angiography of
the renal arteries: technique and evaluation in the study of native and transplant renal
arteries, Br J Radiol 74(878):134–141, 2001.
117. Meijering EH, Niessen WJ, Bakker J, et al: Reduction of patient motion artifacts in digital
subtraction angiography: evaluation of a fast and fully automatic technique, Radiology
219(1):288–293, 2001.
118. Meijering EH, Niesssen WJ, Viergever MA: Retrospective motion correction in digital
subtraction angiography: a review, IEEE Trans Med Imaging 18(1):2–21, 1999.
119. Ashleigh RJ, Hufton AP, Razzaq R, et al: A comparison of bolus chasing and static digital
subtraction arteriography in peripheral vascular disease, Br J Radiol 73(872):819–824, 2000.
120. Schreier DZ, Weaver FA, Frankhouse J, et al: A prospective study of carbon dioxide-digital
subtraction vs standard contrast arteriography in the evaluation of the renal arteries, Arch
Surg 131(5):503–507, 1996.
121. Hawkins IF Jr, Wilcox CS, Kerns SR, et al: CO2 digital angiography: a safer contrast agent for
renal vascular imaging? Am J Kidney Dis 24(4):685–694, 1994.
122. Conlon PJ, Athirakul K, Kovalik E, et al: Survival in renal vascular disease, J Am Soc Nephrol
9(2):252–256, 1998.
123. Textor SC: Progressive hypertension in a patient with “incidental” renal artery stenosis,
Hypertension 40(5):595–600, 2002.
124. White CJ: The renal oculosten(t)otic reflex, Cathet Cardiovasc Diagn 37(3):251, 1996.
125. White CJ, Jaff MR, Haskal ZJ, et al: Indications for renal arteriography at the time of
coronary arteriography: a science advisory from the American Heart Association
Committee on Diagnostic and Interventional Cardiac Catheterization, Council on Clinical
Cardiology, and the Councils on Cardiovascular Radiology and Intervention and on
Kidney in Cardiovascular Disease, Circulation 114(17):1892–1895, 2006.
126. Hood MN, Ho VB, Corse WR: Three-dimensional phase-contrast magnetic resonance
angiography: a useful clinical adjunct to gadolinium-enhanced three-dimensional renal
magnetic resonance angiography? Mil Med 167(4):343–349, 2002.
127. Patel ST, Mills JL Sr, Tynan-Cuisinier G, et al: The limitations of magnetic resonance
angiography in the diagnosis of renal artery stenosis: comparative analysis with
conventional arteriography, J Vasc Surg 41(3):462–468, 2005.
128. Eklof H, Ahlstrom H, Bostrom A, et al: Renal artery stenosis evaluated with 3D-Gdmagnetic resonance angiography using transstenotic pressure gradient as the standard
of reference. A multireader study, Acta Radiol 46(8):802–809, 2005.
129. Tello R, Mitchell PJ, Witte DJ, et al: T2 dark blood MRA for renal artery stenosis detection:
preliminary observations, Comput Med Imaging Graph 27(1):11–16, 2003.
130. Vasbinder GB, Nelemans PJ, Kessels AG, et al: Accuracy of computed tomographic
angiography and magnetic resonance angiography for diagnosing renal artery stenosis,
Ann Intern Med 141(9):674–682, 2004.
CHAPTER
24 Medical and Endovascular
Treatment of Renal Artery Disease
Robert D. Safian, Ryan D. Madder
The clinical diagnosis of renal artery stenosis (RAS) relies on a
high index of suspicion and confirmation by noninvasive and
invasive imaging modalities (see Chapter 23). There are interrelated syndromes associated with RAS, including renovascular
(renin-dependent) hypertension, essential hypertension, reversible
ischemic renal dysfunction, and irreversible ischemic nephropathy.
Clinical features that heighten suspicion for RAS include abruptonset or accelerated hypertension at any age, unexplained acute
or chronic azotemia, azotemia induced by angiotensin-converting
enzyme inhibitors (ACEIs), asymmetrical renal dimensions, and
sudden pulmonary edema in the setting of normal left ventricular
(LV) systolic function. Therapeutic considerations, alone or in combination, include medical therapy, percutaneous revascularization
with angioplasty (PTA) or stenting, and surgical revascularization with bypass surgery or endarterectomy (
Revascularization of RAS with the goal of improving renal function
and blood pressure remains controversial, so patient selection is
extremely important (Fig. 24-1).
Table 24-1) .
General Considerations for Treatment
Atherosclerosis accounts for more than 90% of cases of RAS,
whereas the remaining 10% are associated with fibromuscular
dysplasia (FMD) or inflammatory diseases of the renal arterial circulation. Whereas FMD is typically a disease of young and middleaged females and usually involves the distal two thirds of the renal
artery and its branches, atherosclerotic RAS (ARAS) is a disease
of the elderly, particularly those with diabetes, aortoiliac occlusive disease, coronary artery disease (CAD), and hypertension.
Atherosclerotic RAS usually involves the ostium and proximal one
third of the renal artery, and it is a common manifestation of progressive atherosclerosis.
Despite the prevalence and progressive nature of ARAS, it is likely
many cases are never detected. Most patients with ARAS are identified during evaluation for refractory hypertension or progressive
renal failure, or fortuitously as part of angiographic evaluation for
aneurysmal or occlusive diseases of the aorta and lower-extremity
arterial circulation. In general, decisions about treatment of
patients with ARAS are usually based on blood pressure control,
preservation of renal excretory function, and modification of risk
factors for atherosclerosis.
Identification of Renovascular Syndromes
There are five interrelated renovascular syndromes associated
with RAS that can be broadly classified as anatomical RAS,
renin-dependent hypertension, essential hypertension, reversible
renal ischemic dysfunction, and irreversible ischemic nephropathy.
These syndromes may occur alone or in combination with each
other and with other nonvascular renal diseases. Furthermore,
although the type of RAS (FMD, ARAS) is influenced by age, gender, and other patient-related risk factors for atherosclerosis, clinical manifestations (regarding effects on the kidney, heart, and
brain) may be similar. Renin-dependent hypertension is much
more likely to be caused by FMD in young patients, whereas ARAS
in elderly patients is more likely to be associated with essential
hypertension. Although both FMD and ARAS can be associated
with similar manifestations of injury to the kidneys, heart, and
brain (
Table 24-2), renal revascularization is more likely to cure
hypertension in FMD patients, whereas ARAS patients are likely
to require lifelong antihypertensive medical therapy, despite
1
2
revascularization. The key point is that patients with anatomical RAS without other clinical manifestations may be treated
conservatively without revascularization. Prior to revascularization, patients with RAS and other clinical manifestations should
undergo assessment of renal perfusion and the extent of parenchymal disease to determine the likelihood of clinical benefit.
2
Evaluation of Renal Perfusion
As is true in the coronary circulation, there is poor correlation
between angiographic RAS severity and hemodynamic significance, even when quantitative angiography is used.
angiography alone is insufficient to establish the presence of renal
hypoperfusion, regardless of stenosis severity. Several noninvasive
and invasive methods are available to assess the physiological
impact of ARAS and identify renal hypoperfusion (
see Chapter 23). Nuclear scintigraphy and direct glomerular filtration rate (GFR) measurements can assess single- and total-kidney
blood flow; diminished renal blood flow ipsilateral to a stenotic
renal artery provides reliable evidence of renal hypoperfusion.
Invasively, renal hypoperfusion can be identified with fractional
flow reserve or translesional pressure gradients.
In patients with FMD, angiography alone is nearly useless for
assessment of stenosis severity before or after revascularization,
or for assessment of renal perfusion. In FMD patients, translesional
pressure gradients are extremely useful for localizing the site of
critical stenosis and assessing results after intervention (
Intravascular ultrasound (IVUS) can also be used to assess intraluminal and vessel dimensions, which are nearly impossible to assess
by angiography alone.
3
As a result,
Box 24-1; also
3,7,8
4–6
Fig. 24-2).
Evaluation of Nephropathy
Assessment of baseline parenchymal disease is essential in selecting
patients for renal revascularization (
of parenchymal disease prior to intervention is the most important predictor of adverse outcome. Even if renal hypoperfusion is
present, identification of advanced parenchymal disease suggests
that renal dysfunction maybe irreversible regardless of revascular-
9
ization.
The exception is the patient with advanced parenchymal
disease, bilateral RAS, and recent dialysis, in whom a small increase
in renal blood flow may permit separation from dialysis.
Initial clinical evaluation of parenchymal disease includes serum
creatinine (Cr), urinalysis for proteinuria, and renal duplex ultrasound to measure renal resistive index (RRI) and kidney dimensions. When evaluating baseline renal function in patients with
ARAS, it is important to realize that serum creatinine–based GFR
estimates demonstrate good sensitivity but only modest specificity
for identifying a measured GFR below 60 mL/min/1.73 m2 in individuals with ARAS.
Cr should be performed to evaluate the presence of underlying
nephropathy. Renal resistive index is obtained by averaging values
obtained in the upper, middle, and lower intrarenal segmental arteries according to the formula 100 × [1 − (EDV/PSV)], where EDV and
PSV are Doppler-derived end-diastolic and peak-systolic velocities,
respectively. Compared to patients with RRI less than 80, those with
RRI above 80 are older and have more extensive atherosclerosis
and worse baseline renal function, consistent with more parenchymal disease. Additionally, baseline RRI greater than 80 is associated
with inadequate blood pressure control, worsening Cr clearance,
more frequent progression to dialysis, and higher mortality after
11
As a result, additional testing besides serum
Table 24-3), since the presence
2,10
307
308
Данная книга находится в списке для перевода на русский язык сайта https://meduniver.com/
TABLE 24-1 Therapeutic Options for Patients with Renal Artery Stenosis
TREATMENT IMPACT ON HYPERTENSION IMPACT ON NEPHROPATHY COMMENTS
Medical therapy Effective for control of hypertension, but
most patients require ≥2 medications;
CH
PTA Effective for refractory hypertension in
24
resistant hypertension is common
patients with FMD; not superior to
medical therapy in patients with ARAS
Stents Not evaluated in patients with FMD;
effective for achieving “statistical”
improvement in blood pressure; not
clearly superior to medical therapy
Bypass surgery Not employed for FMD; not clearly useful in
patients with ARAS
ARAS, atherosclerotic renal artery stenosis; FMD, fibromuscular dysplasia; PTA, percutaneous transluminal angioplasty.
No confirmed benefit for reversing or
stabilizing renal function
Uncertain role; complex relationship
between revascularization vs.
complications (distal embolization,
contrast nephropathy)
Same as for PTA; anecdotal experience
suggests benefit if patient does not have
advanced nephropathy
Anecdotal experience suggests possible
benefit in the absence of advanced renal
dysfunction
Mandatory for risk-factor modification
(aspirin, lipid-lowering therapy, smoking
cessation)
Not useful for ostial ARAS because of
suboptimal results
Treatment of choice in most patients with
ARAS if revascularization is needed
Rarely used; perioperative mortality rate
2%-6%
No RAS
Extensive parenchymal disease
Medical
therapy
No
None
Clinical suspicion for evaluation of RAS
(See page 307)
Ye s
Imaging studies to confirm RAS
Ye s
Establish relationship between RAS and end-organ injury
(Table 24-2)
Ye s
Evaluate renal parenchymal disease and renal perfusion
(Box 24-1, Table 24-3)
Renal ischemia,
minimal parenchymal disease
Revascularization
Assess causes of post-procedural renal failure
Arrange long-term follow-up
FIGURE 241 Management algorithm
for patients with atherosclerotic renal
artery stenosis (RAS).
Vital Organ Injury That May Be Caused by
TABLE 24-2
Hemodynamically Significant Renal Artery
Stenosis
ORGAN SYSTEM INJURY
Renal Ischemia/hypoperfusion
Cardiovascular Hypertensive crisis
Cerebrovascular Hypertensive crisis
ACS, acute coronary syndrome; ICH, intracerebral hemorrhage; TIA, transient ischemic attack.
ACS
Unexplained pulmonary edema
Aortic dissection
TIA
Stroke
ICH
Severe retinopathy
Box 24-1 Clinical Evaluation of Renal Artery
Stenosis and Renal Hypoperfusion
Noninvasive Assessment of Renal Blood Flow
125
I-iothalamate GFR (total GFR)
99M
Tc-DTPA (split renal function and single-kidney GFR)
Invasive Assessment of Significance of Renal Artery Stenosis
Percent diameter stenosis by visual estimates or quantitative angiography
Translesional pressure gradient
Fractional flow reserve
IVUS
Renal frame counts
Renal blush score
GFR, glomerular filtration rate;
intravascular ultrasound;
Adapted from Safian RD, Madder RD: Refining the approach to renal artery
revascularization. JACC Cardiovasc Interv 2:161–174, 2009.
125
I-iothalamate, iodine 125–labeled iothalamate; IVUS,
99M
Tc-DTPA, technetium-labeled diethylene-triamine-pentacetate.
2
A B
CD
FIGURE 242 A 71-year-old female with refractory hypertension was found to have right renal artery stenosis (RAS) by noninvasive imaging. Selective
renal angiography demonstrated fibromuscular dysplasia (FMD) of the right renal artery, but stenosis severity was difficult to assess (A). Intravascular ultrasound (IVUS)
revealed complex intraluminal webs (not shown), and the translesional pressure gradient across the diseased segment (black arrows) was 15 mmHg at rest and
20 mmHg after administration of intrarenal dopamine. Angioplasty of the right renal artery (B) did not result in a significant change in appearance by angiography (C)
or (IVUS). After initial balloon angioplasty, the hyperemic translesional pressure gradient remained 20 mmHg. A guidewire pullback revealed a pressure gradient limited
to a focal segment of FMD at the leading edge (black arrowhead). Repeat angioplasty in the proximal right renal artery did not alter the appearance of the artery by
angiography (D), but resulted in complete resolution of the translesional pressure gradient.
309
CH
24
MEDICAL AND ENDOVASCULAR TREATMENT OF RENAL ARTERY DISEASE
TABLE 24-3
Serum Cr Easy to measure and inexpensive. Relatively
Proteinuria Easy to measure and inexpensive. Proteinuria
Renal dimensions Renal length 10-12 cm is generally favorable. Renal
RRI RRI <70 is a good measure of reversibility. Although
Renal arteriogram Preservation of cortical blood flow and absence
Renal biopsy Reliable for histological confirmation of
Cr, creatinine; RRI, renal resistive index.
Adapted from Safian RD, Madder RD: Refining the approach to renal artery revascularization.
JACC Cardiovasc Interv 2:161–174, 2009.
Clinical Evaluation of Renal Parenchymal
Disease
FAC TOR COMMENT
insensitive to degree of renal dysfunction and not
reliable for differentiating nephropathy from renal
ischemia.
≥1 g/24 h is a good indication of nephropathy, but
lesser degrees of proteinuria are less reliable.
length ≤6 cm indicates irreversible renal injury
(atrophic kidney).
RRI >80 indicates parenchymal disease, it should
not be used as the sole indicator of irreversible
renal dysfunction.
of intrarenal arteriolar disease are indicators of
reversible renal dysfunction. Poor cortical blood
flow and severe diffuse intrarenal arteriolar disease
are markers of advanced nephropathy.
nephropathy, but not practical for most patients.
2
renal revascularization.9 Several factors (renal dimensions, serum
creatinine, presence of collaterals, and intact glomeruli by renal
biopsy) have been proposed to suggest reversible renal failure,
but the predictive value of these factors has not been validated,
and renal biopsy is rarely employed for this purpose. Factors that
identify irreversible dysfunction include severe diffuse intrarenal arteriopathy, proteinuria greater than 1 g/24 h (especially in a
diabetic patient), and marked atrophy of the renal cortex.
2
The nephrogram is often overlooked during selective renal
arterio graphy, since many operators tend to focus on the renal
artery itself. However, there are several arteriographic features
that can indicate the presence of nephropathy, including intrarenal arteriolar narrowing, pruning (cut-off) of interlobar
arterioles, and diminished cortical blood flow (
Fig. 24-3). It is
important to understand that it is best to use all the variables
discussed to obtain a “nephropathy profile” because individual
variables alone are not sufficiently reliable to assess the degree
of nephropathy.
2
In the process of evaluating patients, the goal is to differentiate
the impact of ARAS on reversible kidney dysfunction from other
causes of irreversible parenchymal disease, such as diabetic and
hypertensive nephropathy. If renal hypoperfusion is absent, renal
dysfunction is not attributable to ARAS and is more likely due
to intrinsic nephropathy. Also, a patient with unilateral ARAS and
serum Cr over 2 mg/dL is likely to have significant parenchymal disease, and revascularization of such patients may not improve renal
function, especially in the absence of renal hypoperfusion.
Medical Therapy for Renal Artery
Disease
The risk of cardiovascular events in hypertensive adults is most
dependent on the degree of hypertension rather than its cause.
True renovascular hypertension (i.e., renin-dependent hypertension) is much more likely in young patients with FMD than in
elderly patients with ARAS. In fact, most hypertensive patients with
ARAS have essential hypertension, whereas those with accelerated
or malignant hypertension may have a renovascular component
superimposed on a background of essential hypertension.
2
310
Данная книга находится в списке для перевода на русский язык сайта https://meduniver.com/
CH
24
A
B
Patients with FMD rarely have excretory dysfunction, and
hypertension generally responds to ACEIs. In contrast, there are
a number of issues concerning medical management of patients
with ARAS. First, although never specifically studied in patients
with ARAS, it is reasonable to treat all patients with aggressive
risk-factor modification to limit atherosclerosis. These measures include aspirin, lipid-lowering therapy, smoking cessation,
and aggressive treatment of diabetes mellitus to limit diabetic
nephropathy.
with ARAS is similar to that for patients with essential hypertension. Even after renal artery revascularization, antihypertensive
medical therapy is necessary in most ARAS patients, since revascularization cures hypertension (i.e., normal blood pressure off
all medications) in less than 10% of patients.
with ischemic renal dysfunction represent a particularly highrisk group with a poor prognosis, and there are no studies demonstrating benefit of medical therapy for reversing or stabilizing
renal function. The impact of medical therapy on long-term renal
function in ARAS is controversial. One study reported a rise in
serum Cr concentration in 5% to 10% of patients,
12
Second, medical therapy for hypertensive patients
13,14
Third, patients
15
whereas
FIGURE 243 Arteriographic patterns of progressive hypertensive
nephropathy. A, Normal renal
arteriogram and nephrogram (left),
showing excellent cortical blood
flow extending into renal pyramids.
In mild hypertensive nephropathy
(right), cortical blood flow into renal
pyramids is preserved, but there is
diffuse intrarenal arteriolar narrowing
(AA). B, This is a more advanced
stage of hypertensive nephropathy
(left) characterized by diminished
cortical blood flow, some circulation
to renal pyramids (P), and pruning (*)
of several lobar arteries. In end-stage
hypertensive nephropathy (right),
cortical blood flow is absent (CBF), and
there is generalized pruning (*) of most
lobar vessels.
another showed a progressive rise in Cr despite excellent blood
pressure control.
16
Use of an ACEI or angiotensin receptor blocker (ARB) is controversial in hypertensive patients with ARAS. Important considerations relate to extent of RAS and degree of baseline renal
impairment. Patients with hypertension, unilateral ARAS, and normal baseline renal function are good candidates for an ACEI or
ARB. In fact, ACEIs appear to be more effective than other antihypertensive agents in this setting. In patients with hypertension,
unilateral RAS, and abnormal baseline renal function, ACEIs exert
a beneficial impact on survival without affecting renal function.
In these patients, long-term renal function is influenced most by
the degree of baseline renal dysfunction and proteinuria, not
by pharmacological treatment. In diabetic patients with hypertension, unilateral renal artery stenosis, proteinuria, and normal
or abnormal renal function, ACEIs and ARBs are effective antihypertensive agents, and drug-induced reduction of intraglomerular capillary pressure decreases proteinuria and renal injury.
17
It is interesting to speculate whether renal revascularization in
this subgroup of patients could offset the benefit of ACEIs by
increasing intraglomerular capillary pressure, proteinuria, and
renal injury.
In contrast to patients with unilateral ARAS, patients with bilateral RAS (or stenosis in a single solitary kidney) may be especially
sensitive to declines in intraglomerular pressure leading to progressive renal failure. Such changes in intraglomerular pressure
may occur in association with ACEIs or ARBs (due to vasodilation of the efferent arterioles), reduction in intravascular volume
(due to diuretics, dehydration, bleeding), or a decline in cardiac
output due to congestive heart failure (CHF). In studies of thousands of patients with hypertension or CHF (many of whom may
have had occult RAS), discontinuation of ACEI therapy owing to
renal dysfunction was reported in only 0.5% of patients, although
mild to moderate increases in serum Cr were reported in 0.1% to
10%. In contrast, discontinuation of ACEI therapy owing to renal
dysfunction was necessary in 5% to 20% of patients with bilateral
ARAS or stenosis of a solitary kidney.
Taken together, available data suggest that most patients with
unilateral and bilateral ARAS and hypertension will benefit from
an ACEI or ARB. For patients with bilateral ARAS (or stenosis of a
solitary kidney), renal function and serum potassium levels should
be monitored closely during initiation of therapy to identify those
who may be intolerant.
TABLE 24-4
LIMITATION STAR ASTRAL CORAL
N 140 806 1080
Exclude beneficiaries — Yes * Ye s
Assess perfusion No No No
Assess parenchymal disease No No No
Urine protein (mg/day) 140 550 500
RAS <70% 33% 40% NA
Baseline Cr (mg/dL) 1.7 2.0 <3.0
Major renal endpoint EGFR ↓ > 20% 1/Cr 2 × Cr
*Patients who were thought to benefit from renal revascularization were excluded.
†
Patients with refractory hypertension and/or cardiovascular injury were excluded.
Cr, creatinine; EGFR, estimated glomerular filtration rate; NA = not available; RAS, renal artery
stenosis.
From Bax L, Woittiez AJ, Kouwenberg HJ, et al: Stent placement in patients with atherosclerotic
renal artery stenosis and impaired renal function: a randomized trial. Ann Intern Med 150:840–
848, 2009; the ASTRAL Investigators: Revascularization versus medical therapy for renal artery
stenosis. N Engl J Med 361:1953–1962, 2009; and Cooper CJ, Murphy TP,
Matsumoto A, et al: Stent revascularization for the prevention of cardiovascular and renal
events among patients with renal artery stenosis and systolic hypertension: rationale and
design of the CORAL trial. Am Heart J 152:59–66, 2006.
Limitations of Randomized Controlled
Trials of Renal Stenting
†
36
311
CH
24
MEDICAL AND ENDOVASCULAR TREATMENT OF RENAL ARTERY DISEASE
Selecting Patients for Renal Artery
Endovascular Revascularization
The major challenge in selecting patients for renal revascularization is the absence of compelling data supporting doing
so. A review of worldwide studies of ARAS identified approximately 5000 studies of renal revascularization,
two randomized controlled trials (RCTs) of PTA (not stenting) versus medical therapy.
19,20
A subsequent review nearly led
to withdrawal of Center for Medicare and Medicaid Services
(CMS) reimbursement for renal stenting.
two subsequent RCTs,
22,23
and another comparative trial24
reported no benefit of renal revascularization (PTA or stenting) compared to best medical therapy with respect to hypertension control and estimated GFR during 1- to 2-year follow-up.
In contrast, numerous observational studies reported stabilization or improvement in renal function
8,28,29
control
after renal stenting. There are several potential explanations for the negative results of RCTs and discrepant findings
among studies, including treatment of patients with anatomical
stenosis but normal renal perfusion (i.e., oculostenotic reflex),
failure to differentiate reversible ischemic renal dysfunction from
irreversible parenchymal disease (i.e., nephropathy), and unrealistic expectations that ARAS patients have renin-dependent
(i.e., renovascular hypertension) rather than essential hyperten-
2
sion.
In addition, many RCTs have significant methodological
flaws that limit their ability to measure changes in renal function,
raising doubts about the validity of their results and conclusions
(
Table 24-4). Finally, the medical literature is filled with ambiguous
and inconsistent terminology regarding renovascular syndromes.
The 2005 American College of Cardiology/American Heart
Association (ACC/AHA) guidelines propose recommendations for renal artery revascularization,
ommendations have not been established by any randomized
clinical trials. In general, ACC/AHA revascularization guidelines
are based on the assumption that the RAS is hemodynamically significant, and that revascularization will improve blood
pressure control, preserve renal function, or have a favorable
impact on cardiovascular manifestations of severe hypertension. Accordingly, patient selection can be enhanced by identification of clear clinical syndromes that link RAS to reversible
injury to the heart, brain, or kidneys; by demonstration that RAS
causes renal hypoperfusion; and by assessment of baseline
renal parenchymal disease.
18
including only
21
Those two RCTs,
4,25–27
and hypertension
12
even though the rec-
11
The best candidates for revascularization are patients with
RAS, vital organ injury, renal hypoperfusion, and no underlying
nephro pathy. Conversely, the worst patients for revascularization
are those with RAS, advanced nephropathy, and normal renal
perfusion.
2
Vital organ injury includes functional impairment of
the heart, brain, or kidneys attributable to renal artery stenosis;
such manifestations include hypertensive crisis (nonischemic
pulmonary edema, acute coronary syndrome (ACS), aortic dissection, or neurological impairment) and renal insufficiency
(rising Cr due to ACEIs, bilateral ARAS and rising Cr or declining
nuclear GFR, and unilateral ARAS and fractional GFR ≤40%).
Patients with Renal Artery Stenosis
and Refractory Hypertension
In patients with ARAS, refractory hypertension, and normal renal
perfusion, it is reasonable to intensify the antihypertensive regimen, seek alternative etiologies for refractory hypertension, and
follow patients clinically for development of vital organ injury. For
patients with unilateral or bilateral ARAS, refractory hypertension,
and objective evidence of renal hypoperfusion, revascularization
is reasonable if advanced baseline nephropathy is not present
(Fig. 24-4). For patients with hypertension and renal FMD, PTA
should be performed if patients do not respond to ACEIs or ARBs.
Additionally, such patients should undergo carotid duplex ultrasound and intracranial magnetic resonance angiography (MRA)
or computed tomographic angiography (CTA), because carotid
FMD and berry aneurysms of the circle of Willis are common.
2
Patients with Isolated Atherosclerotic
Renal Artery Stenosis
In patients with unilateral or bilateral ARAS and no evidence of
baseline nephropathy or cardiovascular injury, renal perfusion
should be evaluated by noninvasive or invasive techniques. If renal
perfusion is normal, revascularization is not indicated regardless
of stenosis severity; such patients should be followed for development of vital organ injury. If renal hypoperfusion is documented,
such patients may be considered to have “unilateral” renal injury.
This form of renal injury is not mentioned in existing guidelines
and has not been studied in randomized controlled trials, but we
generally consider such patients candidates for renal revascularization to preserve renal function.
2,4
2
312
Данная книга находится в списке для перевода на русский язык сайта https://meduniver.com/
CH
24
FIGURE 244 A 70-year-old man with persistent hypertension despite four antihypertensive medications was diagnosed with bilateral renal
artery stenosis (RAS) (A). Serum creatinine (Cr) was 1.7 mg/dL, and estimated glomerular filtration rate (GFR) was 39 mL/min/1.73 m2. Renal scan demonstrated
symmetrical renal blood flow (49% to right kidney, 51% to left kidney), and measured GFR was 30 mL/min/1.73 m2. Urine collection revealed 500 mg protein in
24 hours, and renal resistive index (RRI) was 82 bilaterally. Renal dimensions were 9.5 cm on the right and 10.0 cm on the left. Selective renal angiography showed
extensive intrarenal arteriolar disease, including pruning of distal vessels, ill-defined renal pyramids, and poor cortical blood flow (B). Medical therapy was adjusted
because of advanced parenchymal disease without renal intervention, and blood pressure normalized.
Patients with Atherosclerotic Renal Artery
Stenosis and Chronic Kidney Disease
Decisions regarding revascularization of patients with ARAS and
renal dysfunction are often challenging.
out renal hypoperfusion should not be revascularized. For patients
with unilateral ARAS, renal hypoperfusion, and underlying nephropathy, decisions regarding revascularization should be individualized; revascularization may not improve renal function but might
be beneficial if other cardiovascular injury is present. Patients with
renal dysfunction and bilateral ARAS or ARAS of a solitary kidney
may have global renal ischemia; such patients should be considered for renal revascularization unless advanced parenchymal disease is identified (
Fig. 24-5). In nondiabetic patients who have been
on dialysis for less than 1 year, it is reasonable to perform diagnostic
testing for bilateral ARAS, since some may benefit from renal revascularization and separate from dialysis.
2
In general, patients with-
2,10
Type of Revascularization
Percutaneous revascularization is now widely accepted as the best
technique for renal revascularization in most patients. For patients
with refractory hypertension and FMD, PTA is preferred and results in
renal artery patency rates of 90% at 10 years.30 Although PTA achieves
excellent results in patients with FMD, stenting is the endovascular
procedure of choice in patients with ARAS. Stenting in ARAS can
be accomplished with procedural success rates exceeding 95%,
major complications in less than 5%, and restenosis in 10% to 15%.
heterogeneous causes of hypertension, varying degrees of renal
dysfunction, inconsistent techniques for revascularization, and
ambiguous terminology and endpoints to assess clinical benefit. For example, hypertension has been classified as “cured”
(i.e., blood pressure is normal without the need for medication),
Impact of Endovascular Revascularization
on Hypertension
The impact of revascularization on hypertension depends on the
type of RAS, presence of renal hypoperfusion, and degree of renal
parenchymal disease.
and two small randomized trials of PTA and medical therapy for
ARAS demonstrated a significant decrease in blood pressure and
fewer medications after PTA,
in hypertensive patients with ARAS showed no difference in outcomes between PTA and medical therapy.
on the impact of renal revascularization on hypertension have
numerous limitations including inclusion of patients with
2
Although numerous observational studies
9,20
a more recent randomized trial
24
Published studies
FIGURE 245 A 69-year-old man with persistent hypertension despite
two antihypertensive medications was diagnosed with unilateral
renal artery stenosis (RAS) by noninvasive imaging. Serum creatinine
(Cr) was 1.1 mg/dL and estimated glomerular filtration rate (GFR) was 63.4 mL/
min/1.73 m2. Renal scan demonstrated abnormal renal perfusion (65% to right
kidney, 35% to left kidney), and measured GFR was 80 mL/min/1.73 m2. There
was no proteinuria, renal dimensions were 12.2 cm on the right and 11.0 cm
on the left, and renal resistive index (RRI) was 62 bilaterally. Selective left renal
arteriography confirmed severe left RAS and a normal intrarenal arteriolar
pattern. Left renal artery stenting was performed because of hypoperfusion of left
kidney and absence of parenchymal disease. Two years later, measured GFR was
86 mL/min/1.73 m2 (53% to right kidney, 47% to left kidney), consistent with
sustained improvement in renal blood flow.
Соседние файлы в папке Библиотека им академика М.И. Перельмана