Renovascular Disease: Diagnosis and Endovascular Therapy

Majdi Aschi, DO, FACC, FCCP

Richard Bright was first to demonstrate an association between hypertension and the kidney. Goldblatt, et al1 were the first to elucidate the pathogenesis of renovascular hypertension, based on animal studies with mechanical renal artery constriction. There is no agreement on how common is renovascular disease and renovascular hypertension. However, the prevalence of renovascular hypertension varies between 0.2% and 32%,2, 3 and it has been reported that less than 0.5% of an entire hypertensive population has renovascular hypertension.4 Dustan, et al, has shown that only 50% of the patients with significant RAS, in fact, had hypertension.7 The only true way to diagnose renovascular hypertension is to correct the renal artery stenosis (RAS) surgically or by endovascular therapy and demonstrate cure of the hypertension. There is a high prevalence (35%-40%) of atherosclerotic renal artery stenosis (ARAS) in patients who have concomitant peripheral vascular disease and/or coronary artery disease.5, 6 High grade bilateral renal artery disease is present in approximately 13% of patients with peripheral and/or coronary artery disease. 5 ARAS has been estimated to be the cause of 10%-15% of new onset end-stage renal disease in individuals over 50 years of age.8, 9

Causes of Renovascular Disease:

  1. Atherosclerosis. Atherosclerosis is involved in about 60%-70% of all renovascular lesions. It usually occurs in the proximal 2 cm of the renal artery. A follow-up hypertension is not a useful marker for the progressive nature of this disease, but serial kidney function and kidney size are.10
  2. Fibrous Dysplasia. Fibrous dysplasia comprises approximately 40% of all renovascular disease. Medial fibrous dysplasia is the most common of the fibrous lesions. Angiographically, medial fibrodysplasia demonstrates a typical "string of beads" in appearance involving the distal two-thirds of the main renal artery and branches.
  3. Renal Artery Aneurysm. There are four types of which saccular aneurysms account for 75% of the aneurysms.11 These aneurysms are specifically of concern when they are greater than 2 cm in diameter, noncalcified and occur in perimenopausal women due to the predisposition to rupture during pregnancy.12
  4. Extrinsic compression by cysts or tumors.
  5. Radiation injury.
  6. Neurofibromatosis.
  7. Vasculitis, i.e., Takayasu's arteritis.
  8. Dissection.
  9. Retroperitoneal fibrosis.
  10. Thromboembolic disease, which may occur as a complication of rheumatic heart disease, infective endocarditis, cardiac operations, renal artery catheterization, etc.

Clinical Clues That Suggest Renovascular Disease or Renovascular Hypertension:

A. High Probability

  1. Malignant or accelerated hypertension. Usually it is greater than 180/100 mmHg and/or resistant to two or more drugs.
  2. Unexplained azotemia, especially after receiving angiotensin converting enzyme inhibitors or angiotensin-II antagonist.
  3. Atrophic kidney or discrepancy in size between the two kidneys (greater than 1.5 cm difference).
  4. Epigastric bruit (systolic/diastolic or prolonged bruit in the flank area).
  5. Unexplained pulmonary edema with or without left ventricular systolic dysfunction.

B. Moderate Probability

  1. Abrupt onset of hypertension before age of 30 or after age 55.
  2. Patients with vascular disease elsewhere (generalized atherosclerosis).
  3. Heavy or prolonged use of tobacco.
  4. Low body mass index.

C. Low Probability

  1. Presentation typical of mild - moderate essential hypertension.

Diagnosis of Renovascular Disease:

Again, the only true way to diagnose renovascular hypertension is to correct renal artery stenosis surgically or by endovascular therapy and demonstrate a cure of the hypertension. Screening tests with the sensitivity below 75% are not recommended. High sensitivity is recommended so those patients with potentially curable forms of hypertension or progressive azotemia are not denied the benefit of an intervention. In adults, there is no usefulness in evaluating renal artery stenosis with intravenous urogram, plasma renin activity, Captopril test, renal vein renin sampling or renal scintigraphy. Renal ultrasound with duplex, spiral CT scanning, magnetic resonance angiography (MRA), intravascular ultrasound (IVUS), conventional angiography, or carbon dioxide angiography (CO2 angiography) are more sensitive and specific and deserve brief review.

Duplex Ultrasonography. Combining B-mode ultrasound with Doppler examinations has proven useful in the diagnosis of RAS. The sensitivity and specificity has been estimated at 89% and 97%, respectively.13, 14 It provides information about the anatomic location of stenosis, an accurate estimate of the kidney size, non-nephrotoxic, nonaltered by placing patients or taking them off of antihypertensive medication, and relatively less expensive than spiral CT, MRA or angiography. Measuring peak systolic velocity (PSV), end-diastolic velocity and the ratio of the PSV in the renal artery to PSV in the aorta, gives it its high sensitivity and specificity. The criticism, however, has been that larger centers results cannot be duplicated. This is true since the technique has a steep learning curve. In our office, we have been able to closely duplicate the Cleveland Clinic results.

Magnetic Resonance Angiography (MRA). It has a sensitivity and specificity for detecting stenosis > than 60% in the range of about 73%-100% and 76%-100%, respectively. 16-20 Thornton, et al21 has reported improved MRA sensitivity (100%), specificity (98%) and accuracy (99%) when using a gadolinium-enhanced breath hold method. MRA is limited by its availability, high cost of gadolinium and limited evaluation of the distal main, segmental and accessory renal arteries. MRA is dependent upon the equipment, software and the technical expertise of the specialist performing the MRA examination.

CT Angiography. Depending on many factors, including technique used, the sensitivity for diagnosing renal artery stenosis is 59% to 92% and specificity 82% to 98%. 22 - 25 Some of its limitations include a large load of dye, especially in patient with pre-existing renal insufficiency, availability of the software and limited evaluation of distal main renal artery and segmental branches.

CO2 Angiography. It has a sensitivity of 83% and a specificity of 99%.26 CO2 or carbon dioxide angiography provides an alternative to conventional angiography of iodinated contrast and its nephrotoxicity. However, it is cumbersome to use and its disadvantages are related to the buoyancy, compressibility and solubility of the gas. The major drawback of CO2 as a contrast agent is that it does not really have the resolution and clarity that are seen with contrast dye.

Intravascular Ultrasound (IVUS). It is not an ideal screening or diagnostic test for RAS. However it is very useful peri-intervention in determining the significance of the lesion, discriminating among atherosclerotic, fibromuscular disease or other causes of RAS.27, 28

Angiography. It is the gold standard for the diagnosis of RAS. It should be done if some form of intervention is warranted. It is more costly than all of the noninvasive tests and it has very small risk due to its invasive nature.

In our practice we follow and recommend this algorithm for the diagnosis and evaluation of RAS.





Indications for Renal Artery Revascularization.

It is indicated in patients with hemodynamically significant RAS (diameter stenosis >50% and/or the presence of >5 mmHg mean pressure gradient across the stenosis) that is judged to be contributing to poorly controlled hypertension or progressive renal failure. The goals of revascularization of RAS are:

  1. Preserve or restore renal function
  2. Cure or improve control of hypertension
  3. Improve or treat the physiologic effects of significant RAS, including angina, CHF, and recurrent flash pulmonary edema.29, 30

Renal Artery Revascularization. Much controversy remains regarding managing patient with RAS and therefore it requires an intensely individualized approach. About 98% of RAS is caused by fibromuscular dysplasia or atherosclerosis. The threshold for endovascular revascularization of fibromuscular dysplasia is lower since there is a high success rate (>95%), lower morbidity and mortality from surgical revascularization and relatively high cure rate from hypertension (about 50%).31 FMD has excellent treatment results with PTA only and without stenting.

The subsequent discussion will focus mainly on ARAS, which constitutes the majority of patients with RAS.

Surgical vs. Percutaneous Revascularization. In the literature, Weibull et al, 32 published the only randomized trial comparing surgical vs. percutaneous revascularization (pre-stent era) with PTA in low risk patients. PTA achieved comparable secondary patency rate as surgery after additional percutaneous intervention for restenosis. The clinical benefit in regard to cure or improvement of hypertension, frequency of major and minor complications, did not differ statistically. Weibull's study used highly experienced surgeons in renal revascularization which are not available in most institutions, used low risk patients, and was in the pre-stent era. There is still a surgical role for renal revascularization in certain situations, i.e., surgical treatment of abdominal aortic aneurysm that involves the renal artery. However, because of the higher surgical cost, morbidity and mortality in most patients with renal artery stenosis and who have other comorbid diseases, the less invasive percutaneous revascularizations and avoidance of general anesthesia, earlier mobilization and shorter hospital stay with equal efficacy, we recommend percutaneous endovascular therapy as a first choice approach.

Is Percutaneous Renal Artery Stenting (PTAS)
Superior to Balloon Angioplasty (PTA) Alone?

Eighty percent of patients with ARAS have ostial, as opposed to nonostial, atherosclerotic lesions. van de Ven, et al33 have published the randomized trial that established the superiority of stenting over balloon angioplasty in the treatment of ostial ARAS, obtaining a much higher primary success rate with significantly lower restenosis rate.

The Outcome of Renal Artery Stenting in ARAS. The outcome of revascularization is usually assessed by the acute technical success and long term patency, and the clinical success in regard to hypertension control, preservation of renal function and complications.

Technical success has been exceeding 95% in most of the recent series of RA stenting (excluding totally occluded renal arteries).34-39 These series varied to the percentage of patients with ostial vs. nonostial, but most had very similar definitions for technical success. Angiographic restenosis rate was between 10%-25% for the Palmaz stent (Cordis, Miami, FL). 34-39 These studies and others failed to delineate as we hope to see in the future, by a multivariate analysis the restenosis rate in relation to vessel size, lesion location, stent length, stent design, technique, plaque burden and patient's comorbidities. In the future, IVUS will be instrumental in doing these studies.

Effect of Revascularization.

  1. Hypertension is cured in about 50% of FMD after revascularization, however in patients with ARAS it is cured rarely, and only in 11% of the patients. Hypertension has been followed in a nonrigorous non-scientific fashion pre- and post-revascularization of renal arteries in most of the published literature. Improved control of hypertension with fewer medications is a more realistic goal. The recent randomized trials40, 41 attempted to compare PTA versus medical therapy for hypertensive patients with ARAS. However, their findings and conclusions revealed a clinically important fall in blood pressure in both groups and that previous uncontrolled and unblinded assessments of PTA over-estimated its potential for lowering blood pressure.
  2. Renal Function. ARAS is a slow, progressive disease. Caps MT, et al 42, 43 employed serial doppler ultrasound and reported cumulative incidents of ARAS progression of 35% at three years and 51% at five years. The tighter the stenosis, the higher the incidence of progression. Progression to occlusion was infrequent (3%). Another study by Caps, et al, 42, 43 used serial doppler ultrasound to demonstrate the association between progression of RAS and loss of renal mass and elevation of serum creatinine. Dorros G, et al., 44 has shown that renal impairment and bilateral renal artery disease have adversely affected survival. In their study of 163 patients who had renal stenting and were followed for four years, the systolic and diastolic pressures improved in about half of their patients and creatinine improved or stabilized in about two-thirds of their patients. The cumulative probability of survival was 74%, ±4% at three years. Survival was normal 92%, ±4% in patients with normal baseline renal function, fair 74%, ±7% for patient with mildly decreased renal function, and poor 52%, ±7% in patients with elevated baseline creatinine (³ 2.0 mg/dl). Thus, early diagnosis and adequate revascularization before the onset of renal dysfunction could be beneficial for blood pressure control, preserving or preventing deterioration of renal function and improve patient survival.

So, in interpreting this data, we use mandated early intervention for hemodynamically significant ARAS, however this strategy means that about half of the patients will receive unnecessary revascularization since half will not have progressed. This is due to our enormous gap in misunderstanding of which patients will progress to loss of renal function and hence, will benefit from the revascularization procedure.

In reviewing the literature, it appears that renal function, as judged by serum creatinine, improves in 20%-30%, stabilizes in 40%-60% and deteriorates in 20%-30% of patients with pre-existing renal insufficiency.33, 35-37, 39,44-49 Harden, et al.,48 has demonstrated that successful stenting, slowed the rate of progression of renal failure in 89% of patients whose creatinine was < 400 umol/l.

Complications. 33-38, 44-47, 49-51 The overall procedure-related mortality is low (<1.0%). Morbidity includes access site complications, renal parenchymal perforation, renal artery dissection, dye induced renal failure, atheroembolic complications. The overall minor and major complication risks range between 10%-15%.

Conclusion

More than 95%-98% of renovascular disease is due to ARAS and fibromuscular dysplasia. The diagnosis is mostly based on the availability of the test and the technical expertise of the technicians and physicians. Endovascular stenting provides safer options than surgery and has a better acute technical result, especially in the treatment of ostial ARA lesions. Stenting improved long-term vessel patency over PTA alone. Revascularization and managing patients with RAS should be individualized. Based on available literature, the select group of patients that appear to derive most benefit from revascularization are:

  1. Dialysis-dependent renal failure patients with RAS and salvageable kidneys.
  2. Global renal ischemia from bilateral RAS or unilateral RAS supplying single functioning kidney and progressed renal failure. Intervention recommended or preferred while creatinine is < 400 umol/l or creatinine <2.0 mg/dl.
  3. Bilateral artery stenosis with recurrent flash pulmonary edema with normal systolic or abnormal diastolic function and/or decreased ejection fraction.
  4. Bilateral RAS with uncontrolled hypertension.

References

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  33. van de Ven PJG, Kaatee R, Beutler JJ, et al.: Arterial stenting and balloon angioplasty in ostial atherosclerotic renovascular disease: a randomized trial. Lancet 1999, 353:282-286. This randomized trial established the superiority of stenting over balloon angioplasty in the treatment of ostial ARAS, obtaining a much higher primary success rate with significantly lower restenosis rate.
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December, 2000/ Jacksonville Medicine

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