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Renal artery stenosis (RAS) is the narrowing of the lining of the main artery that supplies the kidney. Depending on the degree of narrowing, patients can develop hypertension called renal vascular hypertension (RVH). This form of hypertension is the most common cause of secondary hypertension.
RVH occurs when RAS produces a critical narrowing of the artery that supplies one of the kidneys. Critical RAS is defined as at least 70% narrowing of the renal artery, based on angiographic (blood vessel x-ray) evaluation.
Reduced blood flow through the renal artery causes the kidney to release increased amounts of the hormone renin. Renin, a powerful blood pressure regulator, initiates a series of chemical events that result in hypertension. Renal vascular hypertension can be very severe and difficult to control.
The kidney with RAS suffers from the decreased blood flow and often shrinks in size (atrophies). This process is called ischemic nephropathy. The other kidney is at risk for developing damage from the hypertension. Often developing hypertensive nephrosclerosis. The persistent elevated blood pressures in this non-stenotic kidney can cause progressive scarring (sclerosis) leading to progressive loss of filtering function in this kidney as well. Both unilateral (occurring on one side) RAS and bilateral (occurring on both sides) RAS can ultimately lead to chronic renal failure.
Atherosclerotic Renal Artery Stenosis (AS-RAS) and Fibromuscular Dysplasia (FMD)
AS-RAS is due to the build-up of cholesterol on the inner lining of the renal artery. It is exceedingly more common then the unusual case of FMD-RAS.
FMD-RAS
FMD-RAS occurs almost exclusively in women aged 30 to 40 and rarely affects African Americans or Asians. FMD-RAS is due to an abnormality in the muscular lining of the renal artery.
FMD-RAS is often not as well detected on MRA as it is on other non-invasive studies such as, renal scan with ACE-inhibitor challenge, or ultrasound with Doppler interrogation. FMD responds well to angioplasty and stenting. After plasty long-term patency of the lesion is typically seen.
Incidence and Prevalence
Renal vascular disease accounts for less than 1% of all hypertension in people who have moderately increased blood pressure. But in certain high-risk groups, renal vascular disease may be the cause of 10% to 40 % of all hypertension. FMD RAS occurs almost exclusively in women aged 30 to 40 and rarely affects African Americans or Asians.
Risk Factors
Risk factors associated with the development of atherosclerotic RAS include the following:
Carotid artery disease
Coronary artery disease
Diabetes mellitus
Hypertension (high blood pressure)
Obesity
Old age
Peripheral vascular disease (vascular disease in the extremities, e.g., the legs)
Smoking
There is often a familial history of FMD RAS.
Causes
Most RAS is caused by atherosclerosis or "hardening of the arteries." Atherosclerosis is the build up of cholesterol deposits, or plaque, in the lining of the arteries.
Signs and Symptoms
Conditions that may indicate atherosclerotic RAS include the following:
Asymmetrical (differently sized and shaped) kidneys seen on ultrasound
History of calf pain when walking–indicates impaired circulation to the legs
Intolerance of specific antihypertensive medications—angiotensin-I (ACE-I) inhibitors or angiotensin receptor blockers (ARBs)—with a sudden worsening of renal function
More than three antihypertensive medications needed for blood pressure control
New onset of hypertension in a patient over 55
Presence of a bruit (sound or murmur heard with a stethoscope) in the abdomen (e.g., groin), neck, or other area
Sudden worsening of high blood pressure in a patient whose blood pressure had been well controlled, especially if the patient is over 60
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Diagnosis
The diagnostic method used for renal artery stenosis (RAS) is similar to that used for ischemic nephropathy. The physician may also measure and compare the level of renin, (blood pressure-regulating hormone released by the kidneys), within the right to the left renal veins. If the amount of renin that is released by one-side is markedly higher than the other, this identifies a high renin-releasing kidney consistent with RAS.
Treatment
Medication is used to control hypertension (high blood pressure). Blood pressure medications that directly affect the renin angiotensin pathway can be used toe help control blood pressure. ACE inhibitors and angiotensin receptor blockers (ARBs) are often very effective in patients with unilateral RAS. In some cases, patients with RAS are resistant to these medications.
In patients with bilateral RAS, these medications must be used carefully, because they may cause acute renal failure (ARF). If acute renal failure develops (i.e. creatinine increases by more than 30%), the medication is discontinued and the patient is evaluated for bilateral RAS.
Angioplasty and stenting may be used to improve blood flow. The goal is to improve the circulation of blood flow to the kidney and prevent the release of excess renin, which can help to decrease blood pressure. This helps to prevent atrophy of the kidney. In general, patients with AS-RAS should have stenting done because plasty by itself has a very high incidence of re-stenosis.
Surgery to bypass the narrowing may be performed. If the kidney with RAS has atrophied, a nephrectomy, surgical removal of the kidney, may be advised.
Prognosis
Patients with fibromuscular dysplasia (FMD) RAS often have good, long-term results with angioplasty, but those with atherosclerotic RAS frequently experience a recurrence. Even after partial or complete repair of the narrowed blood vessel, most patients still have hypertension, but require less medication to control it.
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RAS
This form of hypertension is the most common cause of secondary hypertension.
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Reduced blood flow through the renal artery causes the kidney to release increased amounts of the hormone renin. Renin, a powerful blood pressure regulator, initiates a series of chemical events that result in hypertension.
Intolerance of specific antihypertensive medications—angiotensin-I (ACE-I) inhibitors or angiotensin receptor blockers (ARBs)—with a sudden worsening of renal function indicate RAS
ACE inhibitors and angiotensin receptor blockers (ARBs) are often very effective in patients with unilateral RAS. In some cases, patients with RAS are resistant to these medications.
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[quote=AAAAA]Reduced blood flow through the renal artery causes the kidney to release increased amounts of the hormone renin. Renin, a powerful blood pressure regulator, initiates a series of chemical events that result in hypertension.
Intolerance of specific antihypertensive medications—angiotensin-I (ACE-I) inhibitors or angiotensin receptor blockers (ARBs)—with a sudden worsening of renal function indicate RAS
ACE inhibitors and angiotensin receptor blockers (ARBs) are often very effective in patients with unilateral RAS. In some cases, patients with RAS are resistant to these medications.
Remember "unilateral" ONLY !!!!!!!!!!!!!
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The general approach to therapy of ischemic nephropathy involves control of hypertension, preferably with ACE inhibitors or angiotensin II antagonists. Unfortunately, these 2 classes of drugs may lead to increased serum creatine levels and hyperkalemia, limiting their utility. In this case, calcium channel blockers are likely the most useful and best-tolerated agents. Initiate strict control of serum cholesterol, which usually requires the use of HMG-CoA reductase inhibitors, as with all conditions associated with ATH. A study by Bianchi et al (2003) suggests that statins, in addition to ACEI and ARBs, may reduce proteinuria and slow the progression of kidney disease
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Angiotensin II antagonists -- Useful for hypertension and heart failure in patients who are intolerant of ACE inhibitors. Many alternative compounds exist with few significant clinical differences
ARB may be used in "some cases" in RAS !
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Restrict conservative treatment in patients with an established diagnosis of IRD to those with absolute contraindications to surgery or angioplasty or to patients who are likely to succumb due to other comorbid conditions before advancing to end-stage renal disease because of IRD. Clinicians must rely on pharmacologic agents (eg, combination of calcium channels blockers to control blood pressure and optimize renal perfusion), accepting the high probability of deterioration in renal function and shortened survival
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ACEI is not really the medication for RAS.
SURGERY IS THE ONLY CHOICE !
All patients with significant (>80%) bilateral stenosis and stenosis in a solitary functioning kidney are candidates for revascularization, regardless of whether they have renal insufficiency. When renal insufficiency is present, patients with unilateral stenosis are also possible candidates for revascularization. The criteria are slightly different depending on the presence or absence of renal insufficiency.
When renal function is normal or nearly normal (prevention of renal insufficiency), specialists recommend revascularization if the patient meets the following criteria:
The degree of stenosis is more than 80-85%.
The degree of stenosis is 50-80%, and captopril-enhanced scintigraphy findings demonstrate an activation of intrarenal RAS.
Conversely, physicians can choose observation instead of revascularization (serial control every 6 mo with duplex scanning, accurate correction of dyslipidemia, use of drugs that block platelet aggregation) when the patient meets the following criteria:
Stenosis is 50-80%, and scintigraphy findings are negative.
The degree of stenosis is less than 50%.
When renal insufficiency is present and the objective is recovery of renal function together with prevention of further renal function impairment, the prerequisites for revascularization are as follows:
The serum creatinine level is lower than 4 mg/dL.
The serum creatinine level is higher than 4 mg/dL but with a possible recent renal artery thrombosis.
When these conditions are satisfied, the authors propose revascularization if the following apply:
The degree of stenosis is more than 80%.
The serum creatinine level is increased after administration of ACE inhibitors.
The degree of stenosis is 50-80%, and the scintigraphy findings are positive.
Restrict conservative treatment in patients with an established diagnosis of IRD to those with absolute contraindications to surgery or angioplasty or to patients who are likely to succumb due to other comorbid conditions before advancing to end-stage renal disease because of IRD. Clinicians must rely on pharmacologic agents (eg, combination of calcium channels blockers to control blood pressure and optimize renal perfusion), accepting the high probability of deterioration in renal function and shortened survival.
Surgical Care: In 1962, Morris et al compiled the first report on a surgical treatment for occlusion of the renal arteries. They described 8 patients with renal failure who underwent revascularization. Six of these patients returned to essentially normal renal function.
Reports from retrospective studies clearly document that surgical revascularization can improve renal function in patients with ischemic nephropathy. In 1993, Rimmer and Genneari reported postoperative improvement (ie, 20% decrease in serum creatinine concentration) in more than half the patients in 9 studies.
Bypass procedures include aortorenal, hepatorenal, splenorenal, and iliorenal conduits constructed with autologous saphenous veins, autologous arteries, or prosthetic material. For atherosclerotic disease, surgeons can also perform atherectomy to improve renal blood flow. In persons with nonatheromatous renal artery disease, surgeons can reconstruct the renal arteries ex vivo and then can reimplant the revascularized kidney. Reilly and coworkers reported an operative mortality rate of only 6% and immediate improvement in the serum creatinine level of 32% of surgical bypass procedures in 35 patients with solitary kidneys. In the last few years, researchers report that the results are more consistent. The largest series suggests that the GFR improved postoperatively in 49-80% of patients with underlying renal failure.
Revascularization
One unresolved issue is how to determine whether revascularization will salvage renal function from a kidney in which the artery is totally occluded.
Features that may predict successful restoration of renal function include the following:
Collateral circulation and nephrogram on angiography findings
Renal length longer than 9 cm
Lateralization of renin secretion
Differential concentration of urine on split-function study results
Spontaneous back-bleeding findings after arteriotomy during surgery
Viable nephrons after biopsy tissue examination
Specialists suggest nephrectomy as a modality of treatment in persons with unilateral RVD; one study compared nephrectomy versus revascularization in 95 patients and 190 kidneys, and revascularization showed a greater response, better management in blood pressure, and a significant improvement in the GFR.
Angioplasty
Angioplasty is effective for treating renovascular hypertension associated with atheromatous lesions. Indicative of this is the decreased rate of referrals for surgical renovascularization of atheromatous renovascular hypertensive nephropathy by the early 1980s (from 41% to 26%). In practical terms, angioplasty can usually limit hospitalization, avoid general anesthesia, and minimize tissue trauma.
In 1987, Ziegelbaum et al compared the outcomes of angioplasty and surgical bypass. The researchers studied 70 elderly patients with atheromatous disease and found that angioplasty caused major complications, including 2 deaths. Renal function improved (ie, >20% decrease in serum creatinine level) in 57.5% of surgery patients but in only 15.8% of angioplasty patients. After 48 months of follow-up, the unassisted patency rate was only 69% in the angioplasty group compared to 100% in the surgical group.
Erdoes et al examined the results of 58 surgical and 18 percutaneous revascularizations in nonrandomized patients. These 2 approaches showed similar operation risk (mortality rate 4.8-5.3%); however, functional improvement (ie, blood pressure, serum creatinine level) and patency of the renal artery were dramatically better in the surgical group compared to the revascularization group after nearly 4 years of follow-up.
van Jaarsveld et al reported the results of a multicenter trial designed to evaluate the relative benefit of angioplasty versus medical therapy for hypertension associated with RVD. They found that both groups had similar decreases in blood pressure, although the patients who underwent angioplasty used one fewer hypertensive medication. While renal function was improved at 3 months in those undergoing angioplasty, the function at 12 months was similar. They concluded that restricting angioplasty to those with atherosclerotic renovascular hypertension persisting despite use of 3 or more antihypertensive medications was prudent. Note that the patients in this trial did not undergo angioplasty with stent placement. In addition, 9% of patients in the medical therapy–only group experienced total occlusion of the affected renal artery on 12-month follow-up angiography.
A randomized study by van de Ven et al that compared percutaneous transluminal angioplasty (PTA) for ostial ATH with PTA with stent (PTAS) showed that PTAS is a better technique compared to PTA to achieve vessel patency in ostial atherosclerotic RAS. The primary success rate was 57% for PTA compared with 88% for PTAS. The restenosis rate after a successful primary procedure was 48% for PTA compared to 14% for PTAS. In the last 6 years, the use of PTAS in patients with ostial stenosis or early restenosis has led to a considerable reduction in the restenosis rate. Controversy still surrounds the best approach to patients with atherosclerotic renovascular disease, as reviewed by Ives et al (2003), Textor (2004), and Plouin (2003).
In some institutions, PTAS is the first-step approach in patients with IRD, and practitioners reserve surgery for the technical failure of percutaneous maneuvers. However, surgery remains the first choice of treatment under certain conditions, including the following:
Simultaneous abdominal aorta aneurysm
Renal artery aneurysm
Renal artery occlusion (with unsuccessful thrombolysis)
Renal artery rupture
RAS secondary to kinking
Peripheral multifocal stenosis
Unsuccessful angioplasty
A small, retrospective review of 20 patients (Dejani et al) who underwent a revascularization procedure (ie, surgery, PTA, PTAS) revealed a high complication rate (increased serum creatinine level in 25%, eosinophilia in 5%, atheroemboli in 15%, renal artery dissection in 5%) despite achieving improved serum creatine values in only 25%. Fifty percent of patients had stable azotemia. The authors and others conclude that a prospective, randomized trial of medical management with or without PTAS is warranted for this complex clinical problem.
Consultations: The optimal approach to therapeutic interventions should be developed in consultation with an interventional radiologist and vascular surgeon to determine the relative expertise of these subspecialists at the individual medical center.
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BE VERY CAREFUL TO START PATIENT ON ACEI with BILATERAL RAS
The pathophysiology behind renal artery stenosis is important to understand since ACEIs and ARBs may impair renal function in patients with this condition. The most common cause of renal artery stenosis (70% of cases) is an occlusion secondary to an atheromatous plaque at the beginning of the renal artery.7 The second type of lesion leading to stenosis is a fibromuscular dysplasia of the renal artery
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VERY IMPORTANT POINT
Of patients with bilateral renal artery stenosis who start on ACEI therapy,
one-third show a rise in Scr (serum creatinine) by more than 30%.12
An acute increase in Scr of 30% or more from baseline, stabilizing within two months of the first dose, has been shown to be associated with the preservation of renal function.11
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Patients at Risk of Significant Decline
in Renal Function From ACEIs and ARBs
Patients with:
• Severe atherosclerotic renal artery stenosis (particularly "bilateral" stenosis)
• Congestive heart failure or renal insufficiency (serum creatinine >1.6 mg/dL) who are hospitalized
• Primary renal disease, including diabetic nephropathy
• Serum creatinine >3.0 mg/dL
• Volume depletion from excess diuresis
• Nephrotic syndrome (severe proteinurea [>3 g/day], hypoalbuminemia, edema, susceptibility to infections)
• Hepatic cirrhosis with ascites
• Gastrointestinal fluid loss
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