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improved (number or dose of medications is reduced, blood pres-
7
1
sure is better controlled, or both), or unchanged. Interpretation of
data is limited by the uncertain clinical relevance of these classification groups. Furthermore, there are several potential reasons
why renal artery revascularization for ARAS may not result in dramatic improvement or cure of hypertension. First, many patients
with ARAS probably have essential, not renovascular hypertension.
Experimental Goldblatt models demonstrate renin-angiotensin
activation due to RAS, but hypertension in humans is more complex than indicated by these models.
31
Hypertension in ARAS may
be confounded by the presence of sympathetic and cerebral nervous system activation, vasoactive oxygen species, abnormalities
in endothelial-dependent relaxation, and ischemic and hypertensive intrarenal injury.
32
A more complex milieu than suggested
by Goldblatt models is suggested by similar degrees of renin activation in hypertensive patients with and without ARAS and
by the low cure rates demonstrated after successful revascularization. Second, many patients with hypertension have intrarenal
parenchymal disease, leading to hypertensive nephropathy and
self-perpetuating hypertension. In these patients, hypertension is
sustained by intrarenal mechanisms including increased sympathetic nerve activity, renin-angiotensin system activity, and impaired
sodium excretion regardless of patency of the proximal renal artery.
Despite these limitations, it is apparent that hypertension is more
likely to be cured after revascularization in patients with FMD
than in those with ARAS (75% vs. < 20%), regardless of the type of
revascularization.
20,30
With respect to differences in unilateral and
bilateral ARAS, one study suggested that improvement in hypertension after renal stenting was more likely in the presence of severe
bilateral ARAS and severe baseline hypertension (mean arterial
pressure >
absent.
in blood pressure when renal hypoperfusion was sought and corrected by renal stenting.
110 mmHg),33 especially when parenchymal disease is
9,34
A contemporary study reports substantial improvement
8
Impact of Revascularization on Renal
Function
Observational studies suggest that renal artery revascularization can
stabilize or improve renal function (
zation results in significant improvement in postoperative total- and
single-kidney nuclear GFR, a slower decline in GFR, and improvements in renal dimensions and hyperconcentration of urinary
creatine. Improvement in renal function after stenting occurred in
8% to 22% of patients in a systematic review,18 and 20 of 22 cohort
studies reported improvement or stabilization of renal function.
Fig. 24-6). Surgical revasculari-
In contrast to these observational data, five prospective randomized trials of renal revascularization failed to demonstrate improvement in renal outcomes after intervention.
19,20,22–24
Interpretation of
these studies is confounded by failure to assess renal perfusion
and the extent of baseline nephropathy prior to revascularization. Additionally, these studies relied on reciprocal serum Cr or
creatinine-based GFR estimates as major renal endpoints, which
have been shown to be unreliable for serial assessment of renal
function in ARAS patients.
11
Taken collectively, these studies suggest
that patient selection for revascularization of ARAS that is based on
the oculostenotic reflex, and without assessment of renal ischemia
and parenchymal disease, is likely not beneficial.
Impact of Revascularization
on Cardiovascular Outcome
Understanding the impact of renal revascularization on longterm outcome is hampered by selection bias and poorly designed
randomized controlled trials. The survival of medically treated
patients with renovascular disease has not been defined, but
most late deaths are due to cardiovascular events rather than progressive renal failure. After revascularization, predictors of 5- and
10-year mortalities include age older than 60 years, CAD, baseline
renal insufficiency, and persistent elevation of postoperative creatinine. Baseline Cr above 1.5 mg/dL is the strongest independent
predictor of late mortality at 4 years (relative risk [RR] 5.0); is a
stronger correlate of late mortality than diabetes (RR 2.5) or age
older than 70 years (RR 1.9); and is associated with a greater risk of
deterioration in renal function.35 Together, these data suggest that
elderly patients with advanced generalized atherosclerosis, manifested by occlusive diseases in multiple vascular beds and baseline renal insufficiency, have a worse prognosis than patients with
limited atherosclerosis and normal renal function. These data also
suggest that the outcomes of renal revascularization are better
when revascularization is performed before the development of
advanced parenchymal disease.
To address the impact of renal artery revascularization on overall cardiovascular outcomes, best medical therapy alone is being
compared to medical therapy plus stenting in the CORAL trial
(Cardiovascular Outcomes with Renal Atherosclerotic Lesions).
Enrollment of approximately 1100 randomized patients is expected
by 2012, and the primary endpoint is a composite of death, myocardial infarction (MI), stroke, hospitalization for congestive heart
failure, need for renal replacement, and doubling of serum Cr at
36
5 years.
Conclusions
313
CH
24
MEDICAL AND ENDOVASCULAR TREATMENT OF RENAL ARTERY DISEASE
Patients with true renin-dependent (renovascular) hyperten-
–3
6
×10
5
4
3
2
1
serum creatinine
0
–600
–500
–400
–300
–200
–100
0
100
200
300
400
500
600
sion are typically young or middle-aged females with FMD. Initial
therapy for renovascular hypertension associated with FMD is
an ACEI; refractory hypertension responds readily to PTA without stenting. In contrast, ARAS is highly prevalent among elderly
patients with other manifestations of atherosclerosis, and frequently results from in-growth of atherosclerotic plaque from
the abdominal aorta, compromising the ostium of the renal
artery. In elderly patients with generalized atherosclerosis and
ARAS, hypertension is usually not renin-dependent (i.e., essential hypertension). Because renal revascularization rarely cures
hypertension, these patients should be treated aggressively with
FIGURE 246 Relationship of reciprocal serum creatinine (Cr)
concentration over time in patient with ischemic nephropathy treated by
stenting. In the 600 days prior to revascularization, renal function deteriorated
progressively. After stenting, the slope of the reciprocal Cr relationship is zero,
suggesting stabilization of renal function. (Reproduced with permission from
Harden PN, MacLeod MJ, Rodger RS, et al: Effect of renal artery stenting on progression
of renovascular renal failure. Lancet 349:1133, 1997.)
Stent inserted
Time (days)
26
antihypertensive medical therapy. Patients with ARAS, hypertension, and functional impairment of the heart, brain, or kidneys
should be considered for renal revascularization. Patients with
renal hypoperfusion should be treated before the development
of advanced renal failure and ischemic nephropathy. The best
candidates for revascularization are those with baseline serum
Cr less than 2.0 mg/dL, bilateral ARAS, normal renal resistive indices, no proteinuria, and one or more manifestations of cardiac,
cerebral, or renal functional impairment. In these patients, renal
revascularization is best accomplished by stenting.
314
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3. Subramanian R, White CJ, Rosenfield K, et al: Renal fractional flow reserve: a hemodynamic
CH
evaluation of moderate renal artery stenoses, Catheter Cardiovasc Interv 64:480–486, 2005.
4. Hanzel G, Balon H, Wong O, et al: Prospective evaluation of aggressive medical therapy
for atherosclerotic renal artery stenosis, with renal artery stenting reserved for previously
24
injured heart, brain, or kidney, Am J Cardiol 96:1322–1327, 2005.
5. Leertouwer TC, Derkx FH, Pattynama PM, et al: Functional effects of renal artery stent
placement on treated and contralateral kidneys, Kidney Int 62:574–579, 2002.
6. La Batide-Alanore A, Azizi M, Froissart M, et al: Split renal function outcome after renal
angioplasty in patients with unilateral renal artery stenosis, J Am Soc Nephrol 12:1235–
1241, 2001.
7. Tonino PAL, De Bruyne B, Pijls NHJ, et al: Fractional flow reserve versus angiography for
guiding percutaneous coronary intervention, N Engl J Med 360:213–224, 2009.
8. Mangiacappra F, Trana C, Sarno G, et al: Translesional pressure gradients to predict
the blood pressure response after renal artery stenting in patients with renovascular
hypertension, Circ Cardiovasc Interv 3:537–542, 2010.
9. 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 344:410–417, 2001.
10. Textor SC, Wilcox CS: Renal artery stenosis: a common treatable cause of renal failure, Annu
Rev Med 52:421–442, 2001.
11. Madder RD, Hickman L, Crimmins GM, et al: Validity of estimated glomerular filtration rates
for assessment of baseline and serial renal function in patients with atherosclerotic renal
artery stenosis: implications for clinical trials of renal revascularization, Circ Cardiovasc
Interv 4:219–225, 2011.
12. Hirsch AT, Haskal ZJ, Hertzer NR, et al: ACC/AHA 2005 Practice guidelines for the
management of patients with peripheral arterial disease, Circulation 113:463–654, 2006.
13. Cooper CJ, Murphy TP: Is renal artery stenting the correct treatment of renal artery
stenosis? the case for renal artery stenting for treatment of renal artery stenosis, Circulation
115:263–270, 2007.
14. Dworkin LD, Jamerson KA: Case against angioplasty and stenting of atherosclerotic renal
artery stenosis, Circulation 115:271–276, 2007.
15. Caps MT, Zierler RE, Polissar NL, et al: Risk of atrophy in kidneys with atherosclerotic renal
artery stenosis, Kidney Int 53:735, 1998.
16. Toto RD, Mitchell HC, Lee HC, et al: Reversible renal insufficiency due to angiotensin
converting enzyme inhibitors in hypertensive nephrosclerosis, Ann Intern Med 115:513,
1991.
17. Remuzzi G, Bertani T: Pathophysiology of progressive nephropathies, N Engl J Med
339:1448, 1998.
18. Balk E, Raman G, Chung M, et al: Effectiveness of management strategies for renal artery
stenosis: a systematic review, Ann Intern Med 145:901–912, 2006.
19. Webster J, Marshall F, Abdalla M, et al: Randomised comparison of percutaneous
angioplasty vs. continued medical therapy for hypertensive patients with atheromatous
renal artery stenosis, J Hum Hypertens 12:329–335, 1998.
20. Plouin PF, Chatellier G, Darne B, et al: Blood pressure outcome of angioplasty in
atherosclerotic renal artery stenosis: a randomized trial, Hypertension 31:823–829, 1998.
21. Balk EM, Raman G: Comparative effectiveness of management strategies for renal artery
stenosis: 2007 update, comparative effectiveness review no. 5 update. (Prepared by Tufts
New England Medical Center under Contract No. 290-02-0022) Rockville, MD, 2007, Agency
for Healthcare Research and Quality.
22. 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.
23. The ASTRAL Investigators: Revascularization versus medical therapy for renal-artery
stenosis, N Engl J Med 361:1953–1962, 2009.
24. Van Jaarsveld BC, Krijnen P, Pieterman H, et al: The effect of balloon angioplasty on
hypertension in atherosclerotic renal-artery stenosis, N Engl J Med 342:1007–1014, 2000.
25. Muray S, Martín M, Amoedo ML, et al: Rapid decline in renal function reflects reversibility
and predicts the outcome after angioplasty in renal artery stenosis, Am J Kidney Dis 39:60–
66, 2002.
26. Harden PN, MacLeod MJ, Rodger RS, et al: Effect of renal-artery stenting on progression of
renovascular renal failure, Lancet 349:1133–1136, 1997.
27. Watson PS, Hadjipetrou P, Cox SV, et al: Effect of renal artery stenting on renal function and
size in patients with atherosclerotic renovascular disease, Circulation 102:1671–1677, 2000.
28. De Bruyne B, Manharan G, Pijls NHJ, et al: Assessment of renal artery stenosis severity by
pressure gradient measurements, J Am Coll Cardiol 48:1851–1855, 2006.
29. Mahmud E, Smith T WR, Palakodeti V, et al: Renal frame count and renal blush grade:
quantitative measures that predict the success of renal stenting in hypertensive patients
with renal artery stenosis, J Am Coll Cardiol Interv 1:286–292, 2008.
30. Slovut DP, Olin JW: Fibromuscular dysplasia, N Engl J Med 350:1862–1871, 2004.
31. Krum H, Sobotka P, Mahfoud F, et al: Device-based antihypertensive therapy: therapeutic
modulation of the autonomic nervous system, Circulation 123:209–215, 2011.
32. Higashi Y, Sasaki S, Nakagawa K, et al: Endothelial function and oxidative stress in
renovascular hypertension, N Engl J Med 346:1954–1962, 2002.
33. Rocha-Singh KJ, Mishkel GJ, Katholi RE, et al: Clinical predictors of improved long-term
blood pressure control after successful stenting of hypertensive patients with obstructive
renal artery atherosclerosis, Catheter Cardiovasc Interv 47:167, 1999.
34. Zeller T, Ulrich F, Muller C, et al: Predictors of improved renal function after percutaneous
stent-supported angioplasty of severe atherosclerotic ostial renal artery stenosis,
Circulation 108:2244–2249, 2003.
35. Dorros G, Jaff M, Mathiak L, et al: Four-year follow-up of Palmaz-Schatz stent revascularization
as treatment for atherosclerotic renal artery stenosis, Circulation 98:642, 1998.
36. 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.
CHAPTER
25 Surgical Management
of Atherosclerotic Renal Artery
Disease
Billy G. Chacko, William B. Newton III, Kimberley J. Hansen
The introduction of new, more potent antihypertensive agents
and percutaneous endovascular techniques has influenced surgical intervention for atherosclerotic renal artery disease (ARAS).
Many physicians currently limit surgical intervention to severe
hypertension despite maximal medical therapy, or disease patterns
not amenable to percutaneous transluminal renal artery angioplasty (PTRA), or renovascular disease associated with excretory
renal insufficiency (i.e., ischemic nephropathy). As a result, the
patient population selected for operative management is often
characterized by bilateral ostial renal artery stenosis (RAS) or occlusion (85%) superimposed on diffuse extrarenal atherosclerotic
disease (91%) in combination with renal insufficiency (60%).
Although there are several operative methods that can correct
ARAS, no single technique is clearly superior. Optimal methods of
operative renal reconstruction vary with the patient, pattern of renal
artery disease, and clinical significance of associated aortic lesions.
1
1–3
Prevalence, Evaluation, and Diagnosis
Prevalence
As discussed in Chapter 23, it has long been recognized that anatomical renal artery disease may be clinically silent. Conversely,
the disease may account for 3% of hypertension within the general
population. Of patients presenting for chronic renal replacement
therapy, 10% to 20% have renal artery disease.
alence in patients with mild hypertension is low, renovascular disease is frequently present in patients with severe hypertension.
Dietch et al. found that 50% of patients aged 60 years or older
with diastolic blood pressure 104 mmHg or higher demonstrated
significant RAS or occlusion.5 When these characteristics were
associated with serum creatinine (SCr) greater than 2.0 mg/dL,
the prevalence of renal artery disease increased to 70%. Half of
these latter patients demonstrated bilateral renal artery disease.
These data suggest that the probability of finding clinically significant renal artery disease varies directly with the patient's age,
severity of hypertension, and severity of renal insufficiency. With
this in mind, we recommend evaluation for renovascular disease in
all persons with severe hypertension, especially when severe hypertension is found in combination with excretory renal insufficiency.
Evaluation
Through continued improvements in software and probe design,
renal duplex ultrasonography is an accurate and reliable method
to identify hemodynamically significant renal atherosclerotic
disease.
renal function, and overall accuracy is not affected by concomitant aortoiliac disease. In addition, preparation is minimal (an
overnight fast), and there is no need to alter antihypertensive
medications.
renal duplex ultrasound examination effectively excludes ischemic nephropathy because the primary consideration is global
renal ischemia based on main renal artery disease affecting both
kidneys. When screening for renovascular hypertension, however, a
negative duplex ultrasound examination does not reliably exclude
surgical disease due to stenotic accessory arteries or branch renal
artery disease.
7,8
The examination poses no risk to residual excretory
When evaluating for renovascular renal insufficiency, a negative
7
Despite enhanced recognition of multiple arteries
4–6
Although its prev-
by color Doppler flow, only 40% of these accessory renal vessels
are currently identified by renal duplex ultrasound examination.
Aortography and renal angiography may be indicated after a
positive duplex ultrasound study in selected patients. Patients
with severe hypertension and negative or nondiagnostic duplex
ultrasound examinations, especially children and young adults,
should also undergo angiography. Diagnostic digital subtraction angiography (DSA) can be performed with minimal risk in
an outpatient setting. In planning open operative therapy, imaging includes lateral aortography to evaluate the mesenteric vessels. Concurrent mesenteric artery disease was identified in 50%
of patients with significant RAS in an angiographic case series
of U.S. veterans.
authors identified a significant and independent association of
mesenteric artery stenosis with renal artery stenosis.10 Concurrent
mesenteric artery disease has bearing on the use of splanchnorenal reconstruction.
9
In an elderly population-based cohort, the
Diagnosis
When a unilateral renal artery lesion is confirmed in an adult
patient with severe hypertension, its functional significance
should be defined. Unfortunately, measurement of renal vein
renin does not have great value when severe bilateral disease
or disease to a solitary kidney is present. Therefore, the decision
for empirical intervention is based on severity of the renal artery
lesions, severity of hypertension, and degree of associated renal
insufficiency. In the latter instance, issues determining recovery
of excretory renal function in patients with ischemic nephropathy remain ill-defined. Our center's experience with over 240
patients with severe hypertension (mean, 201/104 mmHg) and
a preoperative SCr of 1.8 mg/dL or greater has demonstrated a
significant association between improved renal function after
operative intervention and the site of renal artery disease, extent
of renovascular repair, and rate of decline in preoperative renal
function.
in excretory renal function is associated with the best opportunity for recovery of renal function.
improved renal function after operation is the primary determinant of dialysis-free survival among patients with preoperative
ischemic nephropathy.
appropriate as a combined aortic procedure in the absence of
functional studies (e.g., renal vein renin assay) when hypertension
is severe, the patient does not have significant risk factors for operation, and the probability of technical success is certain (>99%).
In these circumstances, correction of a renal artery lesion may be
justified to eliminate all possible causes of hypertension and renal
dysfunction. Because the probability of blood pressure benefit is
lower in such a patient, morbidity from the procedure must also be
predictably low.
cal decision to intervene is based on severity of the renovascular
lesions and degree of hypertension.
disease consists of severe stenosis on one side and only mild or
moderate disease on the contralateral side, the patient is treated as
though only a unilateral lesion exists. If both renal arteries have only
moderately severe disease (65%-80% diameter-reducing stenosis),
renal revascularization is undertaken only if hypertension is severe.
1,2,11–15
Complete renal artery repair after a rapid decline
11,12,14
Most importantly,
14
Surgical repair of unilateral renal artery disease may be
3,16
When a patient has bilateral RAS and hypertension, the surgi-
2,16
If the pattern of renal artery
315
316
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In contrast, if both renal artery lesions are severe (>80% stenosis)
and the patient has resistant hypertension despite medical therapy,
bilateral simultaneous renal revascularization is performed.
Furthermore, at least mild excretory renal insufficiency is often
present. Because renal insufficiency usually parallels the severity
of hypertension, a patient who presents with severe renal insuffi-
CH
ciency but only mild to moderate hypertension usually has renal
25
parenchymal disease. Characteristically, renovascular hypertension
associated with severe renal insufficiency or dialysis dependence
is associated with very severe bilateral stenoses or total renal artery
occlusions.
2,14
When considering repair of renal artery disease, one
should evaluate the clinical status with respect to this characteristic presentation.
Management Options
Management of renal artery disease discovered incidentally during evaluation of cardiac, aortoiliac, or infrainguinal disease is
controversial. In this setting, the decision must address the need
for additional diagnostic tests and the decision whether or not to
perform combined intervention. Advocates for combined intervention frequently cite “natural history” data (
suggest atherosclerotic lesions of the renal artery frequently progress and progression is associated with irretrievable decline in
kidney size and function. Recent experience, however, disputes
this view. In an 8-year follow-up study of Cardiovascular Health
Study participants,
27
no individual with hemodynamically significant RAS at baseline demonstrated progression on follow-up.
Renal artery stenosis at baseline was not associated with a
decline in kidney size or function. In the absence of renovascular
hypertension or insufficiency (i.e., ischemic nephropathy), these
prospective data suggest that incidental renovascular disease
should not be submitted to intervention by any method. This conclusion is supported by the retrospective experience reported by
Williamson et al.
28
No prospective randomized clinical trial compares medical
management, percutaneous renal angioplasty with stent, and surgical reconstruction in patients with atherosclerotic renovascular
disease (also see Chapter 24). In patients with functionally significant renal artery lesions and severe hypertension, contemporary
results of operative management argue for a selective approach
toward renal artery intervention.
1,2
Whether by open surgical repair
or catheter-based methods, indications for intervention are the
same. These include all patients with severe or difficult-to-control
hypertension, especially when associated with renal insufficiency.
Table 25-1) that
Patient age, type of lesion, medical comorbidity, and concomitant
aortic disease must be considered in selecting patients for open
surgical or endovascular management. In the complete absence
of hypertension, renal artery intervention is not recommended by
any method.
Operative Management
GENERAL ISSUES
The presence of severe hypertension is considered a prerequisite for renal artery intervention. In general, functional studies
are used to guide management of unilateral lesions. Empirical
renal artery repair is performed without functional studies when
hypertension is severe and renal artery disease is bilateral or the
patient has ischemic nephropathy.
tic renal artery repair in the absence of hypertension, whether as
an isolated operative or catheter-based procedure or combined
with aortic reconstruction, is not recommended. With the exception of disease requiring bilateral ex vivo reconstructions that are
staged, all hemodynamically significant renal artery disease is corrected in a single operation. Having observed beneficial blood
pressure and renal function response regardless of kidney size or
histological pattern on renal biopsy, nephrectomy is reserved for
unreconstructible renal artery disease to a nonfunctioning kidney
(i.e., <10% function by reno graphy).
structions are preferred over indirect methods because concomitant disease of the celiac axis is present in 40% to 50% of patients,
and bilateral renal artery repair is required in 50%.
repair is associated with a significant and independent increased
risk of eventual dialysis dependence.
intraoperative duplex ultrasound is used to evaluate the technical
results of surgical repair.
29
PREOPERATIVE PREPARATION
Antihypertensive medications are reduced during the preoperative period to the minimum necessary for blood pressure
control. Patients requiring large doses of multiple medications
will often have reduced requirements while hospitalized on bed
rest. If continued therapy is required, vasodilators and selective
β-adrenergic blocking agents are the drugs of choice. If an adult's
diastolic blood pressure exceeds 120 mmHg, operative treatment
is postponed until the pressure is brought under control. In this
instance, intravenous (IV) therapy is administered in an intensive
care setting.
1,12,14
Accordingly, prophylac-
3,7,12,14
Direct aortorenal recon-
3,9
Failed surgical
3
To minimize these failures,
TABLE 25-1 Natural History Studies of Atherosclerotic Renal Artery Stenosis
REFERENCE
Wollenweber
Meaney
Dean
Schreiber
Tollefson
Zierler
Webster
Crowley
Caps
van Jaarsveld
*
Percent of renal arteries with baseline stenosis or stenosis in follow-up.
†
Of eight patients with serial angiography.
From Edwards MS, Hansen KJ: Combined aortorenal reconstruction. In Green RM, editor: Complex aortic surgery, New York, 2008, Informa Healthcare.
17
18
19
20
21
22
23
24
25
26
YEAR
1968 109 252 42 59 — Angiography
1968 39 78 34 36 4 Angiography
1981 41 — 44 17 12 Angiography
1984 85 126 52 44 11 Angiography
1991 48 — 54 53* 9* Angiography
1996 76 132 32 20 7 Duplex ultrasound
1998 30 — — 13
1998 1178 — 30 11 0.3 Angiography
1998 170 295 33 31 3 Duplex ultrasound
2000 50 100 12 20 5 Angiography
NO. OF
PATIENTS
NO. OF RENAL
ARTERIES
MEAN FOLLOWUP
MONTHS
ANATOMICAL
PROGRESSION
% OF PATIENTS
†
PROGRESSION
TO OCCLUSION
% OF ARTERIES
†
0
ANATOMICAL
EVALUATION
Angiography
OPERATIVE TECHNIQUES
A variety of operative techniques have been used to treat renal
artery atherosclerosis. From a practical standpoint, the three
basic operations that have been most frequently used are aortore-
nal bypass, renal artery thromboendarterectomy, and renal arter y
reimplantation. Although each method may have its proponents,
no single approach provides optimal repair for all types of renal
artery disease. Aortorenal bypass, preferably with saphenous vein,
is probably the most versatile technique. However, thromboendarterectomy is especially useful for ostial atherosclerosis involving
multiple renal arteries. When the artery is sufficiently redundant,
reimplantation is probably the simplest technique and one particularly appropriate for combined repairs of aortic and renal
pathology.
Certain measures are used in almost all renal artery operations.
Mannitol is administered IV in 12.5-g doses early, and repeated
before and after periods of renal ischemia, up to a total dose of
1 g/kg patient body weight. Just prior to renal artery occlusion, a
bolus of 100 units of heparin per kilogram body weight is given
intravenously, and systemic anticoagulation is verified by activated
clotting time. Unless required for hemostasis, protamine is not routinely administered for reversal of heparin at completion of the
operation.
Aortorenal Bypass
The most common method of revascularization is aortorenal
bypass (
Fig. 25-1). Three types of material are available for con-
duit: autologous saphenous vein, autologous hypogastric artery,
and prosthetic grafts. The choice of conduit depends on a number of factors. In adults, we preferentially use the saphenous vein.
However, if the vein is small (<
4 mm in diameter) or sclerotic, the
hypogastric artery or a synthetic prosthetic graft may be preferable.
A 6-mm, thin-walled polytetrafluoroethylene (PTFE) graft is satisfactory when the distal renal artery is of large caliber (≥
4 mm) and
provides long-term patency equivalent to that of saphenous vein.
Thromboendarterectomy
In cases of bilateral atherosclerosis of the renal artery origins,
simultaneous bilateral endarterectomy may be the most appropriate procedure. Although endarterectomy may be performed in a
transrenal fashion, the transaortic technique is used in the majority of instances. The transaortic method is particularly applicable
in patients with multiple renal arteries that demonstrate orificial
disease. Transaortic endarterectomy is performed through a longitudinal aortotomy, with sleeve endarterectomy of the aorta and
eversion endarterectomies of the renal arteries (Fig. 25-2). When
combined aortic replacement is planned, the transaortic endarterectomy is performed through the transected aorta (
Fig. 25-3).
When using the transaortic technique, it is important to mobilize
the renal arteries extensively to allow eversion of the vessel into the
aorta. This allows the distal endpoint to be completed under direct
vision.
Renal Artery Reimplantation
After the renal artery has been dissected from the surrounding
retroperitoneal tissue, the vessel may be somewhat redundant.
When the RAS is orificial and there is sufficient vessel length, the
renal artery can be transected and reimplanted into the aorta at a
slightly lower level. The renal artery must be spatulated and a portion of the aortic wall removed, as in renal artery bypass.
Splanchnorenal Bypass
Splanchnorenal bypass and other indirect procedures are also used
as alternative methods for renal revascularization.
30
In general, the
authors do not believe these procedures demonstrate long-term
patency equivalent to direct aortorenal reconstructions, but they
are useful in a selected subgroup of high-risk patients. Subcostal
incisions are used to perform splanchnorenal bypass.
30
The right
and left renal arteries are exposed through medial visceral rotation. A great saphenous vein (GSV) graft is typically used to construct the bypass. Occasionally the gastroduodenal artery on the
317
CH
25
SuRgiCAl MAnAgEMEnT of ATHERoSClERoTiC REnAl ARTERy DiSEASE
FIGURE 251 Technique for endto-side (A-C) and end-to-end
(D) aortorenal bypass grafting.
Length of arteriotomy is at least three
times diameter of artery to prevent
recurrent anastomotic stenosis. For the
anastomosis, 6-0 or 7-0 monofilament
polypropylene sutures are used in
continuous fashion under loupe
magnification. If apex sutures are placed
too deeply or with excess advancement,
stenosis can be created, posing risk of
late graft thrombosis. (From Benjamin
ME, Dean RH: Techniques in renal artery
reconstruction: part I. Ann Vasc Surg
10:306–314, 1996.)
C
A
B
D
318
AB
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CH
25
SMA
SMA
Lft. renal a.
IMA
FIGURE 252 Exposure for longitudinal transaortic endarterectomy is
through standard transperitoneal
approach. Duodenum is mobilized
from the aorta laterally in standard
fashion or, for more complete exposure,
ascending colon and small bowel are
mobilized. A, Dotted line shows location
of aortotomy. B, Plaque is transected
proximally and distally, and with eversion
of renal arteries, atherosclerotic plaque
is removed from each renal ostium.
Aortotomy is typically closed with a
running 4-0 or 5-0 polypropylene suture.
IMA, inferior mesenteric artery; SMA,
superior mesenteric artery. (From Benjamin
ME, Dean RH: Techniques in renal artery
reconstruction: part I. Ann Vasc Surg 10:306–
314, 1996.)
B
C
A
D
FIGURE 253 For aortic repair combined with bilateral ostial stenosis of renal arteries, thromboendarterectomy is most commonly performed
through the divided aorta. (With permission from Edwards MS, Cherr GS, Hansen KJ: Treatment of renovascular disease: surgical therapy. In Hallet JW, Mills JL, Earnshaw J,
Reekers JA, editors: Comprehensive vascular and endovascular surgery, Edinburgh, 2004, Mosby.)
right and splenic artery on the left can be transected and anastomosed directly to the renal artery.
Ex Vivo
Reconstruction
Operative strategy for renal artery branch vessel repair is determined by the required exposure and anticipated period of renal
ischemia. When reconstruction can be accomplished with less
than 30 minutes of ischemia, an in situ repair is undertaken without special measures for renal preservation (Fig. 25-4). When
longer periods of ischemia are anticipated, one of two techniques
for hypothermic preservation of the kidney are considered. These
techniques include renal mobilization without renal vein transection and ex vivo repair and anatomical replacement in the renal
fossa. Ex vivo management is necessary when extensive exposure
will be required for extended periods. For atherosclerotic renovascular disease, ex vivo techniques are most commonly required for
branch renal artery repair after failed or complicated PTRA.
INTRAOPERATIVE DUPLEX ULTRASONOGRAPHY
Provided the best method of reconstruction is chosen for
renal artery repair, the short course and high blood flow rates
characteristic of renal reconstruction favor long-term patency.
Consequently, flawless technical repair plays a dominant role in
determining postoperative success. Intraoperative duplex ultrasonography provides a rapid, safe method of verifying technically flawless repair.
29
Because the ultrasound probe can be
placed immediately adjacent to the vascular repair, high carrying
frequencies may be used that provide excellent B-scan detail sensitive to less than 1-mm anatomical defects. Once imaged, defects
can be viewed in multiple projections during conditions of uninterrupted pulsatile blood flow. Intimal flaps not apparent during
static conditions are easily imaged while avoiding the adverse
effects of additional renal ischemia. In addition to excellent anatomical detail, important hemodynamic information is obtained
from spectral analysis of the Doppler-shifted signal proximal and
distal to the imaged defect.
29
Our technique of intraoperative
assessment with routine participation of a vascular technologist
has yielded a scan time of 7 to 10 minutes and a 98% study completion rate.
31
We have studied more than 800 renal artery repairs with ana-
tomical follow-up evaluation and reported on a subgroup of 249
32
repairs.
Intraoperative assessment was normal in 157, whereas
84 repairs (35%) demonstrated one or more defects by ultrasound imaging. Twenty-five of these defects (10%) had focal
increases in peak systolic velocity (PSV) of 2.0 ms or greater with
turbulent distal waveform and were defined as major. Each major
defect prompted immediate operative revision, and in each case
a significant defect was discovered. Ultrasound defects defined
as minor were not repaired. At 12-month follow-up, renal artery
patency free of critical stenosis was demonstrated in 97% of normal studies, 100% of minor defects, and 88% of revised major
defects, providing an overall patency of 97%. Among the five failures with normal ultrasound studies, three occurred after ex vivo
branch renal artery repair.
Results of Surgical Management
Marone et al. reported on operative management for ischemic nephropathy due to ARAS.
went 104 renal artery revascularizations between 1990 and 2001.
Perioperative mortality was 4.1%. Perioperative morbidity occurred
in 5% of patients. After open surgical repair, 42% of their patients
demonstrated improved early renal function (defined as ≥20%
decrease in SCr), 17% experienced a 20% or more increase in SCr,
and the remaining 41% exhibited no significant change. Improved
renal function was durable among surgical survivors at a mean
follow-up of 46 months, whereas 28% developed worsened function, and 39% remained unchanged. These authors noted that early
renal function response was an accurate predictor of long-term
survival.
The results of Marone et al. are similar to those from the authors’
center. From January 1987 through December 1999, 626 patients
33
Ninety-six patients under-
319
CH
25
SuRgiCAl MAnAgEMEnT of ATHERoSClERoTiC REnAl ARTERy DiSEASE
FIGURE 254 A, An ellipse of vena
cava containing renal vein origin
is excised by placement of a large,
partially occluding clamp. After ex vivo
branch repair, renal vein can then be
reattached without risk of anastomotic
stricture. B, Kidney is repositioned
in its native bed after ex vivo repair.
Gerota fascia is reattached to provide
stability to replaced kidney. Arterial
reconstruction can be accomplished
via end-to-end anastomoses (as here)
or occasionally with a combination
of end-to-end and end-to-side anastomoses (C). (From Benjamin ME,
Dean RH: Techniques in renal artery
reconstruction: part II. Ann Vasc Surg
10:409–414, 1996.)
Chilled solution
Rt. kidney
B
Plastic bag
A
C
320
Proportion alive and dialysis-free
Perioperative Survivors: Product–Limit Estimates
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had operative renal artery repair at our center.
and 246 men (mean age, 65 ±
erosclerotic renovascular disease. Their mean blood pressure was
200 ± 35/104 ±
of 10 years. Preoperative mean and median SCr was 2.6 mg/dL
and 1.7 mg/dL, respectively, with a mean estimated glomerular fil-
CH
tration rate (EGFR) of 40.5 ±
25
with atherosclerosis had widespread extrarenal disease, with 70%
demonstrating at least one manifestation of cardiac disease, and
32% a history of cerebrovascular disease. Overall, 90% of patients
exhibited some clinical manifestation of extrarenal atherosclerosis. Evidenced by SCr 1.8 mg/dL or greater, 49% were considered
to have ischemic nephropathy, including 40 patients who were
dialysis dependent.
Among 720 renal artery reconstructions, aortorenal bypass was
performed in 384 instances, with 204 vein grafts, 159 PTFE grafts, and
21 Dacron prosthetic grafts. Splanchnorenal bypass was performed
in 13 instances. Renal artery reimplantation was performed in
56 instances, whereas renal artery thromboendarterectomy was
performed in 267 instances. Revascularization was combined with
aortic or mesenteric reconstruction in 41% of patients. Of the 776
kidneys that were operated on, 56 required nephrectomy.
Perioperative mortality, defined as in-hospital death or death
within 30 days of surgery, occurred in 23 patients (4.6%). This figure
was comparable to reports from other centers with a large experience in renovascular disease.
lowing bilateral renal artery reconstruction or renal reconstruction
combined with simultaneous aortic or mesenteric artery repair.
Mortality following isolated renal artery repair (0.8%) differed significantly from mortality following combined or bilateral repair
(6.9%). Perioperative mortality was significantly and independently
associated with advanced age and congestive heart failure (CHF).
Blood pressure measurements and medication requirements
at least 1 month after operative intervention were used to define
blood pressure response.3 Among all surgical survivors, 85% were
cured or improved, and 15% were considered failed. When compared with blood pressure improved or failed, blood pressure
cure was significantly and independently associated with an
improved dialysis-free survival. Although improved blood pressure
was associated with significant postoperative decreases in mean
blood pressure and medication requirements (205/107 mmHg
vs. 147/81 mmHg, and 2.8 vs. 1.7 medications), improved blood
pressure was not associated with increased dialysis-free survival.
Product-limit estimates of dialysis-free survival according to postoperative blood pressure response are depicted in
Considering all surgical survivors, renal function increased
significantly after operation (preoperative vs. postoperative
mean EGFR, 41.1 ±
[P <0.0001]). For individual patients, a significant change in
excretory renal function was defined as a change in EGFR of 20%
or more obtained at least 3 weeks after repair. Some 58% of patients
with ischemic nephro pathy (preoperative SCr ≥1.8 mg/dL) were
improved, including 28 patients who were removed permanently
from dialysis; 35% remained unchanged, and 7% had worsened
renal function.
on severe hypertension and rapidly deteriorating renal function,
the proportion of patients who improved increased with increasing severity of preoperative renal dysfunction. Among dialysisdependent patients, 70% were permanently removed from dialysis.
This association with increased preoperative SCr and improved
postoperative renal function was significant (P <0.0001).
Success after renal artery intervention is measured by survival
free of dialysis dependence. Freedom from death or dialysis was
significantly and independently associated with cured compared
with improved or unchanged hypertension. Freedom from dialysis
was also significantly and independently associated with improved
compared with unchanged or worsened postoperative renal
function. Preoperative factors significantly and independently
associated with death or dialysis included diabetes mellitus, severe
aortic occlusive disease, and poor preoperative renal function.
21 mmHg, with a mean duration of hypertension
2,14,31
When patients were selected for surgery based
2
Overall, 254 women
9 years) underwent repair for ath-
23.2 mL/min/m2. As a group, patients
34
All but one death occurred fol-
Figure 25-5.
23.9 mL/min/m2 vs. 48.2 ± 25.5 mL/min/m2
of Time to Death or Dialysis (N=472)
Stratified by Blood Pressure Response to Operation
1.0
0.9
0.8
0.7
0.6
0.5
0.4
0.3
Blood Pressure Response
0.2
0.1
0.0
(N=376)
20 40 60 80
0
FIGURE 255 Product-limit estimates of time to death or dialysis
according to blood pressure response to operation. (From Cherr GS, Hansen
KJ, Craven TE, et al: Surgical management of atherosclerotic renovascular disease. J
Vasc Surg 35:236–245, 2002.)
Cured
Improved
Failed
(N=271) (N=184) (N=113) (N=67) (N=30) (N=8)
100 120 140
Follow–up Time (months)
160
The relationship between each category of renal function
response and dialysis-free survival demonstrated significant interactions with preoperative renal function. An increased risk of death
or dialysis was observed for all patients if there was no improvement in postoperative renal function (
Fig. 25-6A).2 For patients with
unchanged renal function following surgery, an increased risk of
death or dialysis was significantly associated with a preoperative
renal function at the 25th percentile of EGFR or less (i.e., with ischemic nephropathy). These relationships are shown for predicted
dialysis-free survival for 25th percentile and median values of preoperative EGFR according to postoperative renal function response
(see
Fig. 25-6).
2
These associations between renal function response and
dialysis-free survival suggest that the designation of renal function
unchanged after intervention as “preserved” may be misleading.
Patients with ischemic nephropathy unchanged after open surgical repair remain at increased risk for death or dialysis. Similar
data relating renal function response and survival free from dialysis
after catheter-based intervention are not currently available.
Consequences of Operative Failures
Renal artery repairs failed in approximately 4% of patients during follow-up.
intervention was equivalent to that observed after primary
operative intervention. However, patients requiring secondary
renal artery intervention had a significant and independent risk
of eventual dialysis dependence (35% vs. 4%).
reviewed report has examined the dialysis risk associated with
restenosis after catheter-based interventions.
Our experience with failed renal artery repairs reinforces two
important issues. First, the irretrievable loss of excretory renal function observed after failed renal artery repair supports the view that
renal revascularization should be performed for clear clinical indications, not as a “prophylactic” procedure in the absence of either
hypertension or renal insufficiency.
reconstructions in these patients are characterized by prolonged
patency. Early failures of repair reflect errors in surgical technique
or operative judgment.
3
Blood pressure response after secondary operative
3
To date, no peer-
2,13,16
Second, direct aortorenal
321
Predicted Survival Estimates of Time to Death or Dialysis
Predicted Survival Estimates of Time to Death or Dialysis
Preop EGFR = 38 mL/min/m**2 (Median)
1.0
0.9
0.8
0.7
0.6
0.5
0.4
0.3
Proportion alive and dialysis-free
0.2
0.1
0.0
A
EGFR Response
Improved
No Change
0
20 40 60 80
Follow-up Time (months)
Worse
Proportion alive and dialysis-free
100 120 140
B
Preop EGFR = 25 mL/min/m**2 (25th percentile)
1.0
0.9
0.8
0.7
0.6
0.5
0.4
0.3
0.2
0.1
0.0
EGFR Response
Improved
No Change
0
20 40 60 80
Worse
Follow-up Time (months)
100 120 140
FIGURE 256 A-B, Predicted dialysis-free survival according to postoperative renal function response for patients with a preoperative estimated glomerular
filtration rate (EGFR) of 25 mL/min/m2 (25th percentile) or 38 mL/min/m2 (median value). Interaction between preoperative EGFR and renal function response for
dialysis-free survival was significant and independent. (From Cherr GS, Hansen KJ, Craven TE, et al: Surgical management of atherosclerotic renovascular disease. J Vasc Surg
35:236–245, 2002.)
CH
25
SuRgiCAl MAnAgEMEnT of ATHERoSClERoTiC REnAl ARTERy DiSEASE
Surgery After Failed Percutaneous
Transluminal Renal Artery Angioplasty
Our experience with 29 atherosclerotic patients repaired after a
failed PTRA has been reported.
failure of PTRA on methods of secondary surgical management,
and blood pressure and excretory renal function response to
operation.
Secondary operative repair was considered complicated in more
than half of these patients. In all, four nephrectomies were required.
Branch renal artery reconstruction was required in two thirds of
patients. Hypertension after operative repair for failed PTRA was
cured in 7%, improved in 50%, and considered unchanged in 43%.
Compared with patients treated by operative repair only, operative
management following failed PTRA was associated with blood
pressure benefit (57% vs. 89% benefited [P <0.001]).
Summary
With proper patient selection, operative repair of atherosclerotic
renovascular disease results in both improved blood pressure
and renal function. Improvement in renal function is associated
with a significant increase in dialysis-free survival independent
of all other covariates. The application of intraoperative duplex
ultrasonography to assess renal artery reconstruction results in
long-term primary patency exceeding 96%. However, when failure of operative repair occurs, eventual renal function is worsened, culminating in an increased risk of dialysis dependence
and death.
Percutaneous transluminal angioplasty with or without stenting
offers blood pressure benefit similar to operative repair for nonostial atherosclerotic lesions of the main renal artery. However,
cumulative data for ostial lesions associated with ischemic
nephropathy suggest that PTRA with or without endoluminal stenting yields inferior renal function benefit. The common practice
of reporting unchanged renal function as “preserved” or “stabilized” after renal artery intervention may be misleading. Patients
with ischemic nephropathy unchanged after open surgical repair
35
We examined the influence of
remain at increased risk for eventual dialysis dependence and
2,12,14
death.
For these reasons, the authors recommend open operative repair of bilateral ostial atherosclerosis and renal artery occlusion associated with severe hypertension and renal insufficiency
in good-risk patients.
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