Review Interventional Cardiology
ReviewInterventionalCardiologyrenalSelecting patients likely to benefit fromrenal artery stentingPatients with refractory hypertension, progressive ischemic nephropathy andcardiac destabilization syndromes (e.g., flash pulmonary edema) with obstructiveatherosclerotic renal artery stenosis (RAS) are likely to benefit from renal arterystenting. Screening for RAS can be done with Doppler ultrasonography (DUS),computed tomographic angiography (CTA) and magnetic resonance angiography(MRA). There is currently a disparity between the acute procedural success of renalartery stenting (97%) and the derived clinical benefit ( 70%), leading to debateabout which candidates ultimately benefit from renal revascularization. Physiologicmeasurements such as hyperemic/resting translesional gradients are useful to confirmthe severity of renal hypoperfusion and therefore improve the selection of patientslikely to respond to renal artery revascularization. Experienced operators shouldperform renal interventions in order to minimize complications. Primary patencyexceeds 80% at 5 years and surveillance for in-stent restenosis can be done withperiodic clinical, laboratory and imaging follow-up.Jose D Tafur-Soto*,1 &Christopher J White1John Ochsner Heart & Vascular Institute,Ochsner Medical Center, 1514 JeffersonHighway, New Orleans, LA 70121, USA*Author for correspondence:Tel.: 1 504 842 4135Fax: 1 504 842 4465jtafursoto@ ochsner.orgKeywords: chronic kidney disease flash pulmonary edema ischemic nephropathy renalartery stenting renal atherosclerosis renal FFR renovascular hypertensionAtherosclerotic renal artery stenosis (RAS)has been identified as an independent predictor of death in patients with coronary arterydisease [1] . However, the cause-and-effectrelation between RAS and mortality remainsunproven. It is possible that the presence ofRAS is a marker for more diffuse or extensiveatherosclerosis, which would result in morevascular-related deaths. Patients who improvetheir renal function after renal stent placement have significantly better survival ratescompared with those whose renal functiondoes not improve [2] . When selecting patientsfor renal artery stenting, clinical, anatomicaland physiologic data should be consideredto optimize the benefit of revascularization.The AHA/ACC Guideline indications forrenal artery revascularization are shown inTable 1 [3] .Renal hypoperfusion is a strong stimulusfor renal neuro-hormonal activation resulting in renin and subsequent angiotensin II10.2217/ICA.14.6 2014 Future Medicine Ltdrelease. Renin–angiotensin–aldosterone system activation occurs with both unilateraland bilateral (or solitary) renal hypoperfusion[4] . This leads to sodium retention, secondary hyperaldosteronism, vasoconstriction andadverse left ventricular remodeling. Whenrenal artery stenosis is unilateral, the ischemic kidney secretes renin, which leads toincreased angiotensin formation and henceelevation of blood pressure. As blood pressure rises, sodium excretion by the contralateral kidney increases; therefore, there is nosodium retention or subsequent volume overload. This is the mechanism for the hypertensive hyponatremia syndrome seen in unilateral RAS [5] . With bilateral (or solitary) renalartery stenosis, the lack of compensation froma normal kidney in terms of natriuresis leadsto fluid retention, loss of kidney function andcongestive heart failure [6] . Improving renalperfusion should have a normalizing effect onthese physiologic processes.Interv. Cardiol. (2014) 6(2), 167–182part ofISSN 1755-5310167
ReviewTafur-Soto & WhiteTable 1. AHA/ACC Guidelines indications for renal artery tomatic stenosisSolitary viable kidney withhemodynamically significant RASIIbCBilateral hemodynamicallysignificant RASIIbCRAS and accelerated, resistant ormalignant hypertensionIIaBRAS and hypertension withunilateral small kidneyIIaBRAS and hypertension withmedication intoleranceIIaBProgressive CKD with bilateral RASIIaBProgressive CKD with RAS to asolitary functioning kidneyIIaBRAS and chronic renal insufficiencywith unilateral RASIIbCCongestive heart failureRAS with recurrent, unexplainedCHF or sudden, unexplainedpulmonary edemaIBUnstable anginaHemodynamically significant RASand unstable anginaIIaBHypertensionPreservation of renal functionCHF: Congestive heart failure; CKD: Chronic kidney disease; LOE: Level of evidence; RAS: Renal artery stenosis.Adapted from 2005 AHA/ACC practice guidelines for the Management of Patients With Peripheral Arterial Disease [3].Several deleterious metabolic pathways in the poststenotic kidney have been implicated in the progression of this disease including microvascular damage,oxidative stress, inflammation and development offibrosis [7] . The extent and severity of the damage ofthe post-stenotic kidney may play an important role inrenal recovery and outcomes of renal angioplasty. Thereversibility of these processes has not yet been fullyestablished. In a series of 17 revascularized kidneys,despite reversal of renal hypoxia and partial restoration of renal blood flow after revascularization, inflammatory cytokines and injury biomarkers remainedelevated and GFR failed to recover in atheroscleroticRAS [8] .Despite excellent angiographic outcomes achievedwith renal stenting, there is a mismatch betweenangio graphic ( 97%) and clinical ( 70%) success.Renal arterial stent placement has proved to be highlysuccessful. In a meta-analysis including 14 studies(678 patients) dealing with renal artery stenting foreither hypertension or chronic kidney disease (CKD),the initial angiographic success rate was 98% (95%CI: 95–100%) [9] . However, the beneficial clinicalresponse for hypertension was 69%, with a cure rateof 20% and improvement in blood pressure in 49%(Figure 1A) . Renal function improved in 30% and stabilized in 38% of patients with an overall favorable168Interv. Cardiol. (2014) 6(2)response rate of 68% (Figure 1B) [9] . This mismatchbetween 98% angiographic success and approximately70% clinical response can be explained by the factthat some of these RAS lesions were not hemodynamically significant, and/or the symptoms (hypertensionor CKD) are not caused by renal artery stenosis. Thekey to successful clinical outcomes is to try to identifywhich of those patients are likely to benefit from intervention and avoid procedures in those patients unlikelyto benefit.A matched cohort study of patients with atherosclerotic RAS collected over 5 years in two large centerscompared medical therapy only (n 182) with primaryrenal artery stenting plus medical therapy (n 348).Patients with CKD stage 3, 4 and 5 had improvedclinical outcome of 20% or more increase in GFR asopposed to no benefit in CKD stage 1 and 2. It suggested that specific subgroups of patients with atherosclerotic RAS, notably those with a more impaired renalfunction, might have greater benefit in terms of survivaland renal function following r evascularization [10] .Several recent randomized clinical trials haveattempted to determine the clinical benefit of renalartery stenting. However, these trials have been flawedby poor design and the inability to objectively assessthe severity of the RAS. They have failed to selectpatients with hemodynamically significant RASfuture science group
Selecting patients likely to benefit from renal artery stentinglesions that cause renal hypoperfusion. The STARtrial attempted to determine the efficacy and safety ofrenal artery stenting in patients with RAS and creatinine clearance 80 ml/min per 1.73m2. The primaryoutcome of 20% decrease in creatinine clearance wassimilar with renal artery stenting and medical therapyalone. However, 18 out of 64 (28%) patients randomized to stent placement did not actually have a stentplaced and the analysis was made on an intention-totreat basis. Twelve (19%) patients were found to havenon-obstructive stenosis (less than 50%) at the time ofthe procedure [11] .The ASTRAL trial was also seriously flawed [12] . Itincluded patients with clinical suspicion of RAS withimaging-confirmed stenosis in at least one renal artery,in whom the physician was uncertain if that the patientwould benefit from revascularization. This excludedpatients most likely to benefit from revascularization,creating a selection bias against severe RAS. Additionally, there was no objective measurement of RAS, onlyvisual estimation was used, which has been shown to beinaccurate [13] . Overestimation of RAS creates a significant bias against revascularization because these mildlesions are not likely to be causing renal hypoperfusionthat would benefit from intervention. In fact, 40% ofpatients had RAS 70%. Only 83% of patients randomized to revascularization actually underwent renalartery stenting. Also, due to the inexperience of theoperators, the procedural success was 78.6%, which isfar below the 97% success rate expected in clinicalpractice [9] . Moreover, there was a serious complication rate of 9% in the percutaneous revascularizationgroup, which is far higher than the 2–4% reported inprior clinical trials [14–20] (Table 2) . Sixty five percentof the centers enrolled 1 patient per year, indicating avery low procedural volume per site and per operator.ASTRAL inappropriately concluded that the risks ofrenal stenting were not justified by the benefits. A better conclusion would have been that patients with mildRAS do not benefit from renal stent placement.The recently published CORAL trial was open topatients with RAS of at least 60% with uncontrolledhypertension (systolic blood pressure [SBP] 155 withtwo or more antihypertensive medications) or chronickidney disease (eGFR 60 ml/min/1.73m2). Patientswere screened with DUS, MRA or CTA. No hemodynamic measurements were reported (see below).The CORAL trial’s original design had to be alteredalong the way because of slower than expected patientenrollment. A major factor limiting enrollment was alack of equipoise between medical therapy and stentplacement. Patients with severe renal artery lesions, inwhom clinicians recommended revascularization, werenot likely to be enrolled in CORAL, as indicated byfuture science groupReviewHypertensionDorros (n 28)Boisclair (n 100)Blum (n 100)Iannone (n 86)Henry (n 92)van de Ven (n 92)Hennequin (n 100)Rees (n 100)Kuhn (n 80)Wilms (n 100)02040Cured608010080100ImprovedRenal functionShannon (n 100)White (n 100)Harden (n 100)Boisclair (n 100)Iannone (n 86)Henry (n 92)van de Ven (n 92)Hennequin (n 100)Rees (n 100)Kuhn (n 80)02040Improved60StabilizedFigure 1. Rates of improvement after renal artery stenting. Clinicaloutcomes after renal artery revascularization in ten different series forboth (A) hypertension control and (B) renal function.Data taken from [9] .modest average renal artery stenosis of 67% found bythe core laboratory. For those patients enrolled, therewas no statistical difference in the primary outcomebetween medical therapy alone and medical therapyand renal artery stenting [21] . CORAL reinforced theneed for better strategies to select patients likely to benefit from renal artery revascularization.Clinical syndromes resulting from renalhypoperfusionThe first step in selecting patients who may benefitfrom renal artery revascularization is to identify theclinical impact of renal artery hypoperfusion. Renalwww.futuremedicine.com169
ReviewTafur-Soto & Whitestent placement may be indicated for asymptomaticpatients with hemodynamically significant RAS basedupon preserving renal mass, on a case-by-case basis(class IIb, level of evidence [LOE]: C). The main clinical syndromes associated with RAS include renovascular hypertension, ischemic nephropathy and cardiacdestabilization syndromes.Renovascular hypertension(Percutaneous revascularization is reasonable forpatients with hemodynamically significant RAS andaccelerated hypertension, resistant hypertension,malignant hypertension, hypertension with an unexplained unilateral small kidney, and hypertensionwith intolerance to medication [class IIa, LOE: B] [3])(Table 1) . Resistant hypertension is defined as bloodpressure above goal on three different classes of antihypertensive medications, ideally including a diureticdrug [22,23] . Secondary causes of hypertension shouldbe evaluated in such patients.Ischemic nephropathy(Percutaneous revascularization is reasonable forpatients with RAS and progressive chronic kidney disease with bilateral RAS or a RAS to a solitary functioning kidney [class IIa level of evidence: B]. Percutaneous revascularization may be considered for patientswith RAS and chronic renal insufficiency with unilateral RAS [class IIb, LOE: C]) [3] (Table 1) . Ischemicnephropathy is potentially a reversible form of kidneyfailure. If unrecognized it can lead to end-stage renaldisease (ESRD). Some studies suggest that as much as11–14% of ESRD is attributable to chronic ischemicnephropathy from RAS [26] . Renal salvage criteriainclude recent increase in serum creatinine concentration, decrease in GFR during ACEI or ARB treatment,absence of glomerular or interstitial fibrosis on kidneybiopsy, and kidney longitudinal diameter 8.0 cm [27] .In a study with a mean follow-up of 2 years, renal function improved in 34 out of 59 patients (57.6%). Theslope of the reciprocal serum creatinine plot beforerevascularization was significantly associated with afavorable clinical response, suggesting that rapidlyprogressive renal failure is associated with a favorableresponse on renal failure progression after revascularization in patients with vascular nephropathy and renalartery stenosis [28] .Cardiac destabilization syndromes(Percutaneous revascularization is indicated forpatients with hemodynamically significant RAS andrecurrent, unexplained congestive heart failure or sudden, unexplained pulmonary edema [class I, LOE:B]. Percutaneous revascularization is reasonable forpatients with hemodynamically significant RAS andunstable angina [class IIa, LOE: B]) [3] (Table 1) . Exacerbations of coronary ischemia (class IIa, LOE: B)and congestive heart failure (class I, LOE: B) causedby peripheral arterial vasoconstriction and/or volumeoverload can be attributed to RAS. The most widelyrecognized example of a cardiac destabilization syndrome is ‘flash’ pulmonary edema (class I, LOE B) orPickering syndrome [29,30] . Renovascular disease mayalso complicate the treatment of patients with heartfailure by preventing the administration of angiotensinantagonist therapy.The importance of renal artery stent placement inthe treatment of cardiac disturbance syndromes hasbeen described in a series of patients presenting witheither congestive heart failure or an acute coronary syndrome [31] . Successful renal stent placement resulted ina significant decrease in blood pressure and symptomimprovement in 88% (42 out of 48) of patients. Forthose patients who presented with unstable angina,renal artery stenting improved the Canadian ClassSociety (CCS) symptoms at least by one regardless ofconcomitant coronary intervention. In patients presenting with heart failure, the New York Heart Association Class of symptoms improved by at least one alsoindependent of coronary revascularization (Figure 2) .In a study performed in 207 patients with decompensated heart failure, 19% had severe RAS and underwent renal artery stenting with decreased frequency ofcongestive heart failure admissions, flash pulmonaryedema NYHA class symptoms and tolerance to ACEinhibitors (Table 3) [32] .Table 2. Complication rates in renal artery interventions.170Study (year)Patients (n)Death (%)Dialysis (%)Major complications (%)Rocha-Singh et al. (1998)208005.2[15]Tuttle et al. (1997)148004.1[16]White et al. (2005)133000.75[18]Burket et al. (2002)17100.70.7[19]Dorros et al. (2004)1630.601.8[20]TOTAL795 1% 1%2.50%Interv. Cardiol. (2014) 6(2)Ref.future science group
Selecting patients likely to benefit from renal artery stentingReviewNoninvasive lesion stratificationDoppler ultrasound evaluationComputed tomographic angiographyComputed tomographic angiography (CTA) can provide high-resolution noninvasive detection of RASfuture science group1009080Improvement (%)Renal artery Doppler ultrasound, or duplex ultrasound(DUS), is a noninvasive examination useful for screening for RAS. It carries a sensitivity of 84%, specificityof 97% and positive-predictive value of 94% for thedetection of significant RAS [33] . The success of thistechnology is highly dependent on technical skill inperforming the examination.A peak systolic velocity (PSV) 180 cm/s has a 95%sensitivity and 90% specificity for significant RAS.When the ratio of the PSV of the stenosed renal arteryto the PSV in the aorta is 3.5, DUS predicts 60%RAS with a 92% sensitivity [34,35] . Duplex also allowsfollow-up of stent patency in patients that have undergone renal artery stenting; however, criteria for nativerenal artery stenosis overestimates the degree of angiographic in-stent restenosis (ISR). Surveillance monitoring for renal stent patency should take into accountthat PSV and renal to aortic ratio (RAR) obtained byDUS are higher for any given degree of arterial narrowing within the stent. PSV 395 cm/s or RAR 5.1 werethe most predictive of angiographically significant ISR 70% [36] .DUS can be performed without risk to the patient,and there is no iodinated contrast or ionizing radiation required. The main limitations for DUS includeunsatisfactory exams due to overlying bowel gas orlarge body habitus. There is a requirement for a capablesonographer who is allowed enough time to performthe examination.The intra-renal resistive index (RI) is the ratio ofthe peak systolic to end diastolic velocity within therenal parenchyma at the level of the cortical bloodvessels [37] . The RI is a representation of small-vesselglomerulosclerosis. There have been conflicting reportsregarding the usefulness of RI to predict individualpatient response to revascularization. One retrospective study demonstrated that an elevated RI greaterthan 0.80 predicted a lack of improvement in bloodpressure and renal function after revascularization;however, it included balloon angioplasty withoutstent procedures, a strategy that is now recognized asless optimal compared with stenting (see below) [38] .A prospective study of renal stenting in 241 patientswith an elevated RI ( 0.70) showed improvement inblood pressure and renal function after intervention[39] . Patients with a higher RI ( 0.8) actually benefitted more from revascularization than did those withmilder elevations.706050403020100PTCA(n 13)No PTCA(n 7)Unstable angina (CCS)Acute improvementPTCA(n 6)No PTCA(n 22)CHF (NYHA)Sustained improvementFigure 2. Symptoms after renal artery stenting in patients presenting withUA/congestive heart failure.CCS: Canadian Class Society; CHF: Congestive heart failure; NYHA: NewYork Heart Association; PTCA: Percutaneous transluminal coronaryangioplasty; UA: Unstable angina.Adapted from [31] .while supplying 3D angiographic images of the aorta,renal and visceral arteries allowing localization andenumeration of the renal arteries, including accessorybranches [40] . It carries good sensitivity (59–96%) andspecificity (82–99%) for detecting significant RAScompared with invasive angiography [41] . CTA requiresthe administration of 100–150 ml of iodinated contrast and therefore carries the potential risk of contrastinduced nephropathy (CIN), especially in patients withan estimated glomerular filtration rate (eGFR) 60ml/1.73m2, diabetes mellitus or anemia [42,43] . However, as CTA scanner technology advances, spatial resolution will improve, scanning time will decrease and theadministered contrast load may be reduced [44] . Additionally, iso-osmolar contrast media are now availablewith decreased potential for nephrotoxicity [45] . CTAallows following patients with prior stents to detect ISR,an advantage over magnetic resonance angiography(MRA) in which metallic stents generate artifact [41] .Contrast-enhanced MRAThis imaging modality allows localization and enumeration of the renal arteries and characterization ofthe stenosis. When compared with invasive angiography it has a sensitivity of 97% and specificity of 93% fordetection of RAS [46] . MRA does not require the use ofionizing radiation. Limitations for contrast-enhancedwww.futuremedicine.com171
ReviewTafur-Soto & WhiteMRA (CE-MRA) include the association of gadolinium with nephrogenic systemic fibrosis when administered to patients with eGFR 30 ml/1.73m 2 and metalcauses artifacts on MRA; therefore, it is not a usefultest for patients with prior renal stents. Other patientswho are not good candidates for MRA include thosewith claustrophobia or those with implanted medicaldevices (e.g., artificial joints, permanent pacemakers)[47] . MRA-based flow measurements have been postulated to predict clinical outcomes after revascularization [48] ; however, there is still no clinical evidence tosupport the use of this technique to select patients fortreatment.Captopril renal scansThis test is based on the principle that patients withflow-limiting stenosis to the afferent arteriolar vascularbed are dependent on the tone of the efferent arteriole to maintain their glomerular filtration rate. Therefore, patients in whom angiotensin-converting enzyme(ACE) inhibitors such as captopril (efferent arteriolevasodilators) decrease the GFR are more likely tohave hemodynamically significant RAS [49,50] . GFRis measured with renal scintigraphic imaging withtechnetium-99m mercaptoacetyltriglycine (MAG3) ortechnetium-99m diethylenetriaminepentaacetic acid(DTPA) [51] . When captopril renal scans (CRS) werecompared with invasive angiography in a clinicalpractice setting, the sensitivity and specificity were 74and 59%, respectively. The test requires close monitoring of volume status and holding of medicationsthat interact with the renin–angiotensin–aldosteronesystem, which in the clinical practice setting becomesunreliable. Another limitation of the test includes therelative contraindication to the use of ACE inhibitorsin patients with significant azotemia, bilateral RAS orRAS to a single functioning kidney. CRS is not a veryuseful test for screening patients for RAS [52] and is notrecommended by the AHA/ACC guidelines [53] . CRSmay have a more important role in providing additional physiologic information in those patients withknown RAS and in whom the decision to revascularizeis being evaluated.Invasive angiographyInvasive angiography remains the ‘gold standard’ forthe diagnosis of renal artery disease. However, thevisual estimate of the severity of stenosis is inaccurate.When a single operator performed visual estimation ofangiographic diameter stenosis in patients with moderate RAS (50–90% diameter stenosis), the correlationwas poor between the angiographic diameter stenosisand resting mean translesional pressure gradient (r 0.43; p 0.12), hyperemic mean translesional pressure gradient (r 0.22; p 0.44) and renal FFR (r 0.18; p 0.54) (Figure 3) [13] . The 3D anatomy ofthe renal arteries and the inability to obtain extremecranio–caudal angulation during invasive angiography contribute to the inaccuracy of determination ofangiographic severity of RAS. Therefore, physiologicassessment should always be performed with invasiveangiography in moderate lesions.Pressure gradientsResting and hyperemic translesional pressure gradients 20 mmHg, as well as a trans-lesional resting pressureratio of 0.90 (Pd /Pa 0.90) correlate with a significantrise in renin concentration in the ipsilateral renal vein[5455]. Renin secretion from a hypoperfused kidney is akey element in the development of renovascular hypertension and ischemic nephropathy. Several series haveshown improved blood pressure response when treatinglesions with resting or hyperemic pressure gradients 20mmHg [56,57] . Based on these observations, an expertconsensus panel of the AHA recommended that a peaksystolic gradient of at least 20 mmHg, or a mean pressure gradient of 10 mmHg, be used to identify candidatelesions for revascularization in symptomatic patientsTable 3. Results of patients undergoing renal artery stenting for control of recurrenthospitalizations for heart failure and flash pulmonary edema.Renal artery stenting (n 39)PrePostp-valueMean BP (mmHg)174/85148/72 0.001Mean number of BP medications32.50.006Mean creatinine (mg/dl)3.162.650.06ACE inhibitor use15.40%48.70%0.004CHF hospitalizations per year2.40.3 0.001NYHA class symptoms2.91.6 0.001ACE: Angiotensin-converting enzyme; BP: Blood pressure; CHF: Congestive heart failure; NYHA: New York Heart Association.Data taken from [32].172Interv. Cardiol. (2014) 6(2)future science group
Selecting patients likely to benefit from renal artery stenting128HPGBPG1064204550 55 60 65 70 75 80Angiographic diameter stenosisCorrelation coefficient 0.43; p 0.12454035302520151050Renal 0 55 60 65 70 75 80Angiographic diameter stenosisCorrelation coefficient 0.22; p 0.444550 55 60 65 70 75 80Angiographic diameter stenosisCorrelation coefficient -0.18; p 0.54Figure 3. Correlation between visual estimation of diameter stenosis and resting pressure gradient, hyperemic pressure gradient andrenal fractional flow reserve.BPG: Resting pressure gradient; FFR: Fractional flow reserve; HPG: Hyperemic pressure gradient.Reproduced with permission from [13] .with RAS [58] . It is important, however, to understandthe limitations of pressure gradients. They can be unreliable indicators of borderline lesions because the gradient is dependent upon the diameter of the catheterplaced across the lesions, the aortic pressure, the degreeof stenosis, the distal vascular bed and the renal venouspressure. The catheter itself can introduce an artificialgradient [59] . Measurements can be done with either a4-Fr catheter or a 0.014” pressure wire. Some authorshave suggested that the later is a more reliable measure;however, they have compared their measurements toangiographic minimal luminal diameter [60] .Hyperemia has been proposed as a way to increasethe accuracy of the pressure measurements, as is thecase in the coronary arteries. Renal hyperemia can beachieved with papaverine [13,55] , dopamine [57] or acethylcholine [61] (see Table 4). Nevertheless, renal hyperemia is lower when compared with the myocardium:renal artery flow reserve is 1.8 compared with 5 or 6 inthe coronary vasculature [62] . The limited renal hyperemia explains why the predictive value of mean restinggradient is similar to that of mean vasodilator-inducedgradient. However, vasodilators increased the gradient,allowing identification of hemodynamically significantlesions in the case of resting gradients 20 mmHg [57] .Hyperemic measures should be performed when resting gradients are not significant and there is persistentsuspicion of renal hypoperfusion.vascular bed. Under conditions of maximum hyperemia (i.e., maximum vasodilation), the flow throughthe conduit artery is maximal, while the resistance ofthe vascular bed is at a minimum and constant. Anyreduction in flow under these conditions is caused bythe stenosis and is proportional to the ratio of pressuredistal to the stenosis (Pd) and the pressure proximal tothe stenosis (Pa).FFR is measured after induction of maximumhyperemia. Renal hyperemia can be obtained withpapaverine, dopamine and acethylcoline. Translesionalpressure gradients are measured and FFR (Pd /Pa) is calculated using a 0.014’’ pressure guidewire. Renal arteryFFR correlates well with other hemodynamic parameters of lesion severity [55,63] (Figure 4) and in someseries has been proven to be a better predictor of clinical response. In one study, renal FFR was measuredafter renal stent placement in 17 patients with refractory hypertension and moderate-to-severe (50–90%stenosis), unilateral RAS. Ten patients had normalbaseline renal FFR (defined as FFR 0.80), whereasan abnormal baseline renal FFR ( 0.80) was recordedin seven patients. At 3 months after intervention, 86%of patients with an abnormal renal FFR experiencedimprovement in their BP, compared with only 30%of those with normal renal FFR (p 0.04) (Figure 5) .Baseline systolic, mean or hyperemic translesionalpressure gradients were not different between patientswhose BP improved and those in whom it did not [64] .Renal artery FFRAnother method to determine the severity of angiographic RAS is to quantify the FFR. This measure ofpressure, which is widely used in the coronary circulation, is based on the principle that flow across a conduitartery is proportional to pressure across the vascularbed and inversely proportional to the resistance of thefuture science groupIntravascular ultrasonographyIntravascular ultrasonography (IVUS) can complement angiography by providing additional informationon lumen dimension and stent expansion, aiding inoptimizing outcomes after intervention. Primary stentpatency is dependent upon maximal size of stents andwww.futuremedicine.com173
Tafur-Soto & White110.950.950.90.90.850.850.8Renal FFRRenal 5051015BPGCorrelation coefficient -0.76; p 0.001605101520 25 30 35 40HPGCorrelation coefficient -0.94; p 0.000145Figure 4. Correlation between fractional flow reserve, and (A) resting pressure gradient and (B) hyperemicpressure gradient.BPG: Resting pressure gradient; FFR: Fractional flow reserve; HPG: Hyperemic pressure gradient.Reproduced with permission from [13].IVUS allows safe selection of the larger stent that fitsthe patient [65] (see below in the ‘Optimizing outcomes’section).For diagnostic purposes, IVUS with virtual histology (VH) has enabled tissue characterization of atherosclerotic plaque [66] and the plaque compositionin coronary plaques detected by VH-IVUS has beenassociated with impairmen
unilateral small kidney IIa B RAS and hypertension with medication intolerance IIa B Preservation of renal function Progressive CKD with bilateral RAS IIa B Progressive CKD with RAS to a solitary functioning kidney IIa B RAS and chronic renal insufficiency with unilateral RAS IIb C
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