More evidence needed for renal artery stenting.
Despite showing promise over the past decade, renal artery stenting has yet to be widely accepted. According to Dr Christopher J Cooper, University of Toledo, OH, this is because role of renal stenting is not yet defined, ‘except in very clear circumstances’. Speaking at this year’s TCT conference in Washington DC, Cooper said that stenting does have its place, but is often seen as inferior to medical therapy. The situations in which stenting is deemed suitable are: occluded or nearly occluded renal arteries and when renal failure is acute, and when anti-hypertensive medical therapy due to severe renal artery stenosis with a significant effect on function. However, in most situations involving normalisation of blood pressure (with or without medical therapy) improvement in renal function and the prevention of clinical events and stenting has not been proven to benefit the patient. He stated that much progress has been made over the past decade, particularly in the areas of establishing adequate non-invasive detection, creating techniques to minimise aortic and renal trauma, improving stents and delivery systems, and forging acceptable long-term patency of stents. “We need to recognise, at least at this point, that there is no randomised trial data available for the benefit of stenting on blood pressure, renal function or clinical events, although there are ongoing multi-centre randomised trials.” Trials such as STent placement and blood pressure and lipid-lowering for the prevention of progression of renal dysfunction caused by Atherosclerotic ostial stenosis of the Renal artery stenosis (STAR) trial, Angioplasty and STent for Renal Artery Lesions (ASTRAL) and Cardiovascular Outcomes with Renal Atherosclerotic Lesions (CORAL), should provide much need evidence.
Although there have been many improvements in diagnostic and interventional techniques, a particular concern is that renal embolization occurs and is responsible for renal deterioration. Renal protection using filter devices capture the emboli thus preventing deterioration, however, it is unclear whether renal protection is really necessary. At a debate at the recent CIRSE meeting in Athens, Greece, Drs Tony Nicholson, Leeds, UK, and Andrew Holden, Auckland, New Zealand outlined the evidence for renal protection. Nicholson, arguing against the motion, “Renal protection is necessary in renal stenting”, began the debate by stating that not all renal embolization causes renal deterioration. Muscle biopsies in patients undergoing angiography have shown subclinical cholesterol embolisation in 25% of cases and cholesterol can be found in renal biopsies where there is no intervention. According to Nicholson, there is little evidence to suggest incidence of renal insufficiency following intervention. In 24 published series including over 1,100 patients (who had undergone percutaneous transluminal angioplasty, with or without a stent), there was a 1% incidence of permanent renal insufficiency, 3.3% incidence of temporary renal insufficiency and segmental infarction in 1.3%, but less than 1% was significant. Furthermore, in a paper by Henry et al. (Journal of Endo Surgery. 1999;6:42-) of 269 patients undergoing renal artery stenting there were no incidences of clinically significant renal insufficiency. Nicholson then assessed whether embolization can be prevented during balloon occlusion. Again, citing a paper by Henry et al. (Journal of Endo Surgery. 2001;8:227–237), it was reported that there were no incidences of renal insufficiency after using an atherembolic renal protection device, in a cohort of patients undergoing renal stenting for ostial atheroma. He then cited his opponent’s own work (Journal of Vascular Surgery. 38(5): 962–8, 2003) that assessed the effect of distal protection on procedure-related acute deterioration in renal function. The outcomes showed 95% of patients stabilised or improved and no patients had acute post-procedural deterioration which, claimed Nicholson, is better than in most reports in the literature. He concluded that there is no evidence at the present time for renal protection devices during intervention and said the importance for adequate hydration cannot be overemphasised. Holden started by outlining the indications for renal artery revascularisation; renovascular hypertension (with normal renal function) and ischaemic nephropathy. In an assessment of the literature, he added that meta-analyses of available randomised controlled trials (RCTs) have failed to show benefit of angioplasty in improving or preserving renal function, although the RCTs were not designed to do so. Holden claims there as two major reasons for the disappointing results reported for stent revascularisation in ischaemic nephrology: poor case selection and poor technique. He said that not all patients were chronic renal ischaemia and renal artery stenosis will respond to revascularisation, but by identifying favourable clinical responders results can be significantly improved. In addition, embolization from local atheroma is caused by poor technique, with many studies reporting acute procedure- related deterioration in renal function of 10–20%. Whilst other causes such as contrast nephropathy, reperfusion damage or arterial dissection may contribute, the most likely cause is embolisation of atheromatous debris (cholesterol athero-embolization), which is known to complicate many interventions (atheromatous aorta, coronary saphenous vein graft, carotid bifurcation and ex vivo renal artery ostium). One of the few RCTs to assess embolic protection devices is the RESIST (Randomized Comparison of Safety and Efficacy of Renal Stenting) trial, a seven-centre, prospective study in which 100 patients undergoing stenting to treat renal artery stenosis received either the platelet inhibitor abciximab (ReoPro) or placebo, and off-label use of the AngioGuard embolic protection device (Cordis) or not. The primary endpoint was change in glomerular filtration rate (GFR) from baseline to one month, a follow-up period deemed long enough to permit resolution of any adverse renal effects of the contrast agent but short enough to avoid confounding effects of restenosis. The GFR declined by 10% in the control group, by 12% in those with AngioGuard only, and by 10% with abciximab only. In contrast, GFR rose by a highly significant 9% in the group given both AngioGuard and abciximab. The second major finding in RESIST was that platelet-rich thromboemboli were found in the filters much more commonly than anticipated, and abciximab sharply curbed this phenomenon. Holden also commented on the two types of protection device currently used: a distal filter that maintains flow to a kidney already damaged by ischaemia throughout the revascularisation procedure; and a distal occlusion balloon that potentially prevent very small particles (<100μm) from embolizing. Interestingly, the current combined length of the filter-balloonstant systems are between 30 and 35mm. As the main renal artery is ~40mm long, early branching can occur in 20–30% of adults. In conclusion, Holden said embolic protection is not recommended in patients with normal renal function. However, outcomes in the ischaemic nephrology group can be improved with appropriate patient selection. There is strong evidence that athero-embolization occurs frequently during endovascular intervention (RESIST data) and there is a high yield of embolic debris within the distal filters. He ended by stating that there is early evidence that embolic protection improves outcomes in the ischaemic nephrology group – however, more RCTs are needed.