Do endovascular specialists have the same level of awareness regarding contrast-induced nephropathy (CIN) as those working in the coronaries?

Probably not, which may be one of the reasons I was invited to speak [at VEITHSymposium]. My interest in CIN began about 12 years ago, partly driven by a patient who presented with an ischemic leg as the result of an embolization from an aneurysm. She had normal renal function on arrival, had a CT scan and a peripheral angiogram within a few hours of each other, and the next day she had a creatinine of 6 and had to go on dialysis for a few weeks. 

Certainly research on CIN in the peripheral and aortic circulation is limited. We have done some work in this area and published it in recent years. But endovascular specialists as a whole probably aren’t as aware of the risks as they should be. It is slightly complicated in the aortic field, because CIN is not the only factor leading to renal failure. For example, after a fenestrated aortic graft, there is manipulation of wires and catheters around the renal artery origin, and stents are being placed into the renal artery. Also in aortic work, there are other mechanisms at play along with the contrast media, so it may be more difficult to tease out how much the contrast is influencing the renal outcome and how much other factors are influencing renal outcome. While there is increasing awareness among endovascular specialists, I think there would be many cases where CIN is something they wouldn’t even think about. In our practice, we are now quite careful with patients coming in for CT scans if they have poor renal function. We tend to admit those patients undergoing aortic procedures with high creatinines prior to intervention. We will pre hydrate them overnight also before CT scanning. But I suspect these are practices that are not in widespread use.  

What is important to consider when evaluating patients for the risk of CIN?

The evidence is quite clear, from the coronary literature, that patients at greatest risk are the ones with current renal impairment before the administration of contrast, so people with established renal disease, diabetics, and then patients having higher contrast doses. Age is also an important factor, because we see increasing incidence of CIN with increasing age. There are a few other factors such as emergency procedures and cardiac failure that also play a role. But the four factors I would highlight are age, existing renal disease, diabetes, and contrast volume. Increasing contrast volume will inevitably increase the incidence of CIN.

What do we know about preventing CIN?

Despite a great deal of work in this area, most of which has been in the coronary circulation, the only proven beneficial therapeutic strategy is to use saline pre hydration, which is fairly clear-cut. People have looked many different therapeutic agents to see if they have a potential role. The one that has been most studied is N-acetylcysteine, and as more data has become available, it has become clear that there is not a huge amount of benefit, if any, to using N-acetylcysteine in CIN. A meta-analysis¹ demonstrated good evidence for initiating statin use pre contrast administration; it may reduce risk by an absolute relative risk of 0.47, which is significant. That meta-analysis involved quite a few publications, over 3,000 patients, and various different statin doses and formulations. It appears that statins themselves are beneficial. Most of our patient population would be on statins anyway. The real question in terms of research going forward is, what dose and which statin? And should you give a higher dose immediately prior to contrast administration? There is work to be done in that area, but certainly I would recommend statin treatment prior to contrast. Vitamin C or ascorbic acid is slightly less well studied and potentially beneficial in the coronary population. A reasonable number of studies have looked at vitamin C, with a smaller number of patients. A meta-analysis one of my team members published last year in JACC confirmed the benefit of vitamin C prior to contrast administration.² The patient numbers are still relatively small despite the meta-analysis suggesting a relative risk of 0.67. 

There is no doubt that CIN is increasing in terms of its incidence, and we are performing more and more complex endovascular procedures in locations such as the aorta with large contrast volumes. At present, there is not much in the literature regarding the aortic and peripheral circulation and reducing the risk of CIN, which may be much higher in this patient group. For patients having complex aortic procedures, it is potentially a very high risk and there is probably an underreported incidence of renal injury. 

What are some of the techniques that might be useful in the periphery to reduce contrast volume?

In the periphery, it is beneficial to use carbon dioxide if you can, so we will use CO2 in lieu of a contrast agent if appropriate. CO2 can be used in the aorta as well. For complex fenestrated aortic grafts, we will use half-strength contrast — reducing contrast strength by diluting it — simple things like that. Potentially, it can help, but you do have to be careful reducing contrast dose. I have observed a case where interventionalists were trying to minimize contrast use in an aortic procedure to such an extent that the imaging wasn’t good enough and a renal artery was inadvertently covered.  

There are also other options out there that may be beneficial, but evidence to support their use is fairly limited. One is a device called the Benephit renal infusion system (AngioDynamics) that goes up from the groin and deploys two catheters into the renal arteries.³ It perfuses drugs directly into the renal arteries to protect the kidneys at times of subsequent contrast administration. 

Any final thoughts?

Most of the work on CIN is being done in the coronary circulation, but people with peripheral vascular or arterial disease are at greater risk of CIN. Endovascular specialists are using more contrast and treat more people with advanced renal failure. There is a great deal of potential for further research into CIN in the aortic and peripheral circulation.  At the moment, we need to raise the profile of the problem, so more people become aware of it. 

References

1. Xie H, Ye Y, Shan G, Zhang S, Fang Q, Yang D, Zeng Y. Effect of statins in preventing contrast-induced nephropathy: an updated meta-analysis. Coron Artery Dis. 2014 Nov; 25(7): 565-574.
2. Sadat U, Usman A, Gillard JH, Boyle JR. Does ascorbic acid protect against contrast-induced acute kidney injury in patients undergoing coronary angiography: a systematic review with meta-analysis of randomized, controlled trials. J Am Coll Cardiol. 2013 Dec 10; 62(23): 2167-2175.
3. Weisz G, Filby SJ, Cohen MG, Allie DE, Weinstock BS, Kyriazis D, et al. Safety and performance of targeted renal therapy: the Be-RITe! Registry. J Endovasc Ther. 2009 Feb; 16(1): 1-12.