{"id":4265,"date":"2018-04-26T13:18:19","date_gmt":"2018-04-26T12:18:19","guid":{"rendered":"http:\/\/www.thinkkidneys.nhs.uk\/aki\/?p=4265"},"modified":"2018-12-03T15:33:04","modified_gmt":"2018-12-03T15:33:04","slug":"first-do-no-harm-what-now-for-contrast-induced-aki-prophylaxis","status":"publish","type":"post","link":"https:\/\/www.thinkkidneys.nhs.uk\/aki\/blog\/first-do-no-harm-what-now-for-contrast-induced-aki-prophylaxis\/","title":{"rendered":"First do no harm\u2026. What now for contrast-induced AKI prophylaxis?"},"content":{"rendered":"

It has been widely agreed for many years that iodine-based radiological contrast can cause AKI, particularly in those patients who are deemed high risk. \u00a0However, as newer research is published, the risk of developing AKI from contrast, may now not be as significant as first thought, with some authors even questioning its existence! \u00a0Part of the problem is that many studies in the past, attributed any change in creatinine in the days following contrast exposure, to the contrast, rather than taking into account other factors e.g. critical illness or simply that the creatinine variation seen, was a normal fluctuation. \u00a0This may have overestimated the incidence of contrast-induced AKI (CI-AKI). \u00a0Also, with greater awareness of AKI and patient risk factors nowadays and the universal use of safer lower osmolar contrast agents, the risk that contrast poses, has reduced even further.<\/p>\n

In the CG169 document in 2013, NICE recommended that intravenous volume expansion should be offered as prophylaxis to anyone who was to receive iodinated contrast agents, if they were at increased risk of AKI or had acute illness.1<\/span> \u00a0The recommendations were made to use a regimen of 0.9% saline or sodium bicarbonate. \u00a0The exact fluid and fluid rates, unfortunately, were never standardised, with considerable variation seen in prophylactic regimens offered globally. \u00a0No proposed prophylactic intervention had ever been compared to that of placebo, with many studies producing conflicting results. Also, patients with low eGFR <30 ml\/min\/1.73m3<\/span> and those who were critically ill, were often excluded from such studies.<\/p>\n

In late 2017, the AMACING study<\/span> compared no CI-AKI prophylaxis to intravenous fluid expansion with 0.9% saline in patients who were high risk for AKI (eGFR of 30-59 ml\/min\/1.73m3<\/span>).2<\/span> \u00a0In this single centre study, 660 patients were recruited who received contrast selectively as part of their investigations. \u00a0Serum creatinine was observed between day 2 to 6 and day 26 to 35 and compared to baseline pre-procedure. \u00a0The results showed that CI-AKI was recorded in 2.6% of the no prophylaxis group and in 2.7% in those who received 0.9% saline hydration. \u00a0No difference in outcomes was found between the two groups with no prophylaxis being cost saving through reduced treatment and hospitalisation costs. \u00a0No haemodialysis or related deaths occurred within 35 days. \u00a05.5% of patients, however, had complications associated with IV hydration, such as symptomatic heart failure (4.0%), hyponatraemia (0.3%) and arrhythmias (1.2%). \u00a0Not receiving prophylaxis was non-inferior and cost saving in preventing CI-AKI compared with IV hydration.<\/p>\n

This study prompted an amendment to NICE guidance, which highlighted that routine use of intravenous hydration therapy prior to contrast in high-risk patients (eGFR 30-59 ml\/min\/1.73m3<\/span>) may not be beneficial and may inadvertently cause harm through fluid overload.<\/p>\n

In another trial, the PRESERVE study<\/span> recruited nearly 5000 patients from the US, Australia, Malaysia, and New Zealand scheduled to undergo angiography.3<\/span> \u00a0All patients were randomly assigned, in a 2-by-2 factorial design, to receive intravenous 1.26% sodium bicarbonate or 0.9% saline plus oral N-acetylcysteine (NAC) or placebo. \u00a0The primary outcome was a composite of death, need for dialysis, or an increase over baseline of at least 50% in serum-creatinine level 90 days post-angiography. \u00a0The study concluded that among patients at high risk for renal complications who were undergoing angiography, there was no benefit of intravenous sodium bicarbonate over intravenous sodium chloride or of oral NAC over placebo for the prevention of death, need for dialysis, or persistent decline in kidney function at 90 days or for the prevention of CI-AKI.<\/p>\n

What do we do now?<\/span> \u00a0 It is likely that routine CI-AKI prophylaxis through intravenous fluid expansion is harmful and costly if done as a \u2018blanket rule\u2019 for any patients\u2019 who have risk factors for AKI. \u00a0No hydration overall was associated with much less patient morbidity and cost! \u00a0It therefore cannot be recommended for use in everyone. \u00a0However, CI-AKI probably does exist but is not as prevalent as first thought. \u00a0Efforts should still be made to limit contrast exposure if appropriate and to individualise preventative measures to those with multiple risk factors, although more research is needed on what effective preventative measures should be offered! \u00a0The PRESERVE study would suggest that there is no role for sodium bicarbonate and\/or NAC over saline therapy.<\/p>\n

In patients with low eGFR <30 ml\/min\/1.73m3<\/span> and those who are critically ill, it is difficult to know exactly what to do. \u00a0Such patients have been excluded from many studies and results cannot be easily extrapolated. \u00a0It would be reasonable until further research is conducted, to try and limit contrast exposure to only when necessary and to ensure that critically ill patients are at least euvolemic and that IV hydration is offered peri-procedure using a crystalloid. \u00a0In critically ill patients at risk of fluid overload, judicious use of volume replacement is recommended. \u00a0Routine AKI preventative measures should still be continued such as good medicines management (e.g. avoiding NSAIDS) and optimising blood pressure. <\/a><\/p>\n

First do no harm!<\/span> \u00a0In our efforts to reduce or stop CI-AKI, it is such a shame, despite best intentions, that we have this double-edged sword and have inadvertently caused significant harm through fluid overload, which may be worse and more prevalent than the CI-AKI that we are trying to prevent!<\/p>\n

iSpyAKI<\/p>\n

<\/p>\n

References:<\/span><\/p>\n

1. \u00a0<\/span>National Institute for Health and Care Excellence (NICE). \u00a0Acute kidney injury: prevention, detection and management. \u00a0Clinical guideline [CG169] Published date: August 2013. <\/span>https:\/\/www.nice.org.uk\/guidance\/cg169<\/span><\/a><\/p>\n

2. \u00a0<\/span>Nijssen EC, Rennenberg RJ, Nelemans PJ, et al. \u00a0 Prophylactic hydration to protect renal function from intravascular iodinated contrast material in patients at high risk of contrast-induced nephropathy (AMACING): a prospective, randomised, phase 3, controlled, open-label, non-inferiority trial. \u00a0Lancet. 2017 Apr 1;389(10076):1312-1322. doi: 10.1016\/S0140-6736(17)30057-0. Epub 2017 Feb 21.<\/span><\/p>\n

3. \u00a0<\/span>Weisbord SD, Gallagher M, Jneid H, et al. for the PRESERVE Trial Group. \u00a0Outcomes after Angiography with Sodium Bicarbonate and Acetylcysteine. \u00a0N Engl J Med 2018; 378:603-614. doi: 10.1056\/NEJMoa1710933<\/span><\/p>\n

 <\/p>\n

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