Renal artery stenosis

Caused by atherosclerosis, fibromuscular dysplasia, vasculitis, neurofibromatosis, congenital bands, extrinsic compression, radiation or scar formation of the renal artery.

90% of cases due to atherosclerosis.

Lesions typically involve the ostium and or the proximal one third of the renal artery and often the adjacent aorta.

In advanced cases segmental and diffuse intrarenal atherosclerosis may be seen.

Highly prevalent in patients undergoing coronary angiography, particularly those with hypertension.

The major cause of renovscular hypertension.

May account for 1-10% of cases of hypertension in the U.S., yet the incidence is more than 30% among patients undergoing cardiac catheterization, and more than 50% in elderly patients with known atherosclerotic disease.

Reported prevalence in Medicare population is 0.5% overall and 5.5% amng patients with chronic kidney disease.

Since patients are asymptomatic the true frequency is probably higher than appreciated.

Prevalence of atherosclerotic RAS increases with advancing age and with the presence of cardiovascular risk factors.

Using duplex ultrasound for screening in the elderly the frequency rate is 7% in a community study (Hansen KJ).

Rate of death about 16% per year.

May be the cause of chronic renal insufficiency and end-stage renal disease.

Progression atherosclerotic renal artery stenosis occurs in more than one third of patients, but the stenosis leads to occlusion in only 3-15% of patients treated medically (Caps MT).

In a study of 170 patients with RAS the cumulative incidence of disease progression was 51% five years after diagnosis (Caps MT et al).

in a review of five trials 49% of all renal arteries examined demonstrated progression of stenosis during a follow-up from 6 to 180 months (Greco BA, Breyer JA).

Most commonly caused by atherosclerosis.

As the lumen of the artery narrows renal blood flow decreases and comprises renal function.

Renal blood flow is 3-5 times greater than the perfusion to other organs, as it drives glomerular capillary filtration.

Renal blood flow and glomerular capillary hydrostatic pressure are important determinant to the glomerular filtration rate.

Causes chronic renal blood flow obstruction and causes changes in the kidney and particularly the tubular tissues.

Renal changes associated include atrophy of the kidney, decreased tubular cell size, inflammation, fibrosis, tubulosclerosis, atrophy of the glomerular capillary tuft, Bowman capsule thickening and intraarterial medial thickening.

The frequency of hypertension from renal or restenosis is unknown.

Impaired renal function is common in patients with atherosclerotic disease, and occlusion of the renal arteries is associated with loss of renal size and function, yet there is little or no correlation between the severity of stenosis and renal function, except when occlusion is present.

The GFR that results is related to the autoregulation system, including angiotensin and other modulators, between the afferent and efferent arteries of the kidney.

When renal perfusion pressure drops below 70-85 mm Hg the GFR will fall.

Lumen narrowing exceeds 50% when autoregulation fails and GFR decreases.

The degree of stenosis that justifies radiographic or surgical correction attempts is not known.

Ratio of arterial pressure in the distal stenosis site of less than 90% of aortic pressure is associated with increased renin release from the affected kidney.

Decreased renal artery perfusion results in increased production of renin, which promotes conversion of angiotensinogen to angiotensin I, which is converted to angiotensin II by angiotensin I converting enzyme, which also inactivates kinins that promotes hypotension.

The largest stores of angiotensin I converting enzyme is present in the pulmonary vasculature, where it plays an important role in systemic blood pressure regulation.

Angiotensin II promotes hypertension by increasing vasoconstrictive activity, and promotes hypertension by increasing total blood volume through its effect on aldosterone and potentially aiding vasoconstrictor response to circulating norepinephrine.

Angiotensin II associated with proinflammatory and toxic cardiovascular effects, including myocardial fibrosis, arterial medial hypertrophy, smooth muscle proliferation and plaque rupture.

Renin has nephrotoxic and vascular toxic effects.

RAS associated with oxidative stress.

Activation of the sympathetic and CNSs, increased blood volume via aldosterone, and direct pressor effects of angiotensin II in the setting of atherosclerotic renal artery stenosis contribute to hypertension.

RAS results in diproportionate cardiac morbidity to the degree of hypertension.

Consequences are hypertension that is difficult to control and progressive ischemic nephropathy.

Atherosclerotic RAS causes progressive loss of renal mass and function over time and in eight group of patients with renal vascular hypertension and 60% abstraction, renal atrophy occurred in 21% of patients(Erdos EG).

Manifests as renovascular hypertension, ischemic nephropathy, and cardiac destabilization syndromes of flash pulmonary edema, or refractoty heart failure, and unstable angina.

Data suggests up to 27% of patients with atherosclerotic or eight as will develop chronic renal failure within six years (Wol thelenweber J et al).

14% of patients in whom dialysis was initiated for end stage renal disease had atherosclerotic RAS (Harding MB et al).

In a Medicare retrospective analysis patients with renal artery stenosis had an increased rate of chronic kidney disease 25%, vs. 2% among those without renal artery stenosis, and coronary artery disease 67% vs. 24% without renal artery stenosis, vascular disease, 56% vs. 13% and stroke 37% vs. 12%.

The presence of RAS predicts adverse coronary events with a higher incidence of hospitalization for angina, myocardial infarction, and coronary artery revascularization (Edwards MS et al or that are).

5-22% of advanced renal disease in patients over the age of 50 years related to ischemic nephropathy.

Occurs frequently inpatient with generalized vascular disease.

Treatment focused on correcting renal artery stenosiswith endovascular revascularization having gradually replaced open surgical techniques.

Renal artery angioplasty reduces the morbidity associated with surgical revascularization and allows high risk patients to have repair that could not undergo surgery.

Patency rates are higher than 90% at five years following open renal artery reconstruction.

Revascularization is performed for about 16% of newly diagnosed patients with atherosclerotic renovascular disese (Kaltra PA).

The Angioplasty and Stenting for Renal Artery Lesions (ASTRAL) trial compared revascularization (95% with stents) with medical therapy to medical therapy alone: a randomized, unblinded trial of 806 patients with RAS: during 5 year study rate of renal impairment indicated no significant benefits with respect of renal function, blood pressure, renal events, cardiovascular events or mortality (ASTRAL investigators).

In the ASTRAL study serious complications including deaths and amputations occurred in 23 patients of 280 patients treated with revascularization

Meta-analysis of three randomized studies indicated that there was no evidence of worthwhile clincial benefit for angioplasty, as compared to medical therapy, and was linited to slight improvement in blood pressure (Ives NJ).

In a non-atherosclerotic renal artery disease Ham and colleagues demonstrated open surgical reconstruction as more durable intervention and improved patency compared with percutaneous treatment of such diseases which include Taakayasu arteritis and fibromuscular dysplasia (Ham et al).

Screening imaging tests include MRA, CT Angiography, Doppler ultrasound, renal scan, and angiography.

Screening peripheral renin levels and renal vein renin samples have been utilized.

For screening purposes renal vein sampling, perpheral renin levels, renal scans are not sensitive or specific enough to be recommended.

Renal artery imaging is optimal if it can detect renal artery stenosis on the basis of anatomic and hemodynamic severity, identify consequences of renal artery stenosis on the artery and the associated kidney, identify shrinkage of the renal parenchyma with a kidney being less than 8 cm, and the demonstration of functional data with enhanced imaging and assessment of viability of renal parenchyma and abilities to establish the criteria associated with renal impairment.

Typically ultrasound is the first imaging study used to detect RAS.

Ultrasound results in RAS is operated dependent, with accuracy ranging from 60-90%.

Ultrasound can provide information on the size of the kidneys, the presence of renal functional reserve, renal resistive index ( defined as peak systolic velocity – end diastolic velocity/peak).

A high renal artery and diastolic velocity of greater than 90 cm/s and the low renal resistive index of less than 75-80, indicate no microvascular disease or increased resistance.

Nonrandomized studies suggested revascularization improves renal function in approximately 25% of patients with RAS (BonnelliFS, Mckusick, MA).

Increased velocity on US is a marker of hemodynamicallly significant stenosis.

Renoaortic velocity ratio (renal artery peak systolic velocity/aortic peak velocity) greater than 3.5 correlated to 60% stenosis (Olin JW et al).

Renal artery peak systolic velocity greater than 150 cm/s correlates to 50% stenosis, and a velocity greater than 180cm/s correlates to 60% stenosis.

US has a sensitivity and specificity of 85% and 92%, respecdtively in detecting hemodynamically significant RAS.

Fibromuscular dysplasia associated RAS can be optimally managed with balloon angioplasty.

Treatment has evolved from balloon angioplasty, which was marginally effective, to present management of balloon expandable stent placement, which can yield patent renal arteries more than 95% of the time.

Renal stent placement is superior to balloon angioplasty on the basis of randomized trials and meta-analysis.

Renal stents are effective for lowering blood pressure and for ischemic nephropathy.

Renal stents are not as effective in patients with lesions of less than 50% stenosis with out a translational pressure gradient.

Renal stents are useful in the presence of bilateral renal artery stenosis and/pulmonary edema.

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