Intravenous Contrast Medium–induced Nephrotoxicity: Is the Medical Risk Really as Great as We Have Come to Believe? 1
ABSTRACT From the multiple perspectives described, it is our belief that the risk of CIN with CE CT has been exaggerated. Clinical rates and adverse outcomes from cardiac catheterization and intervention cannot be extrapolated to the clinical experience with CE CT. It appears that all currently used nonionic CM have similar safety profiles. We believe that modern CM pose only a small risk to renal function and that thresholds of creatinine above which CM are withheld for CT should be increased to improve the accuracy of CT examinations. The population of patients with mild to moderate renal dysfunction who would then receive CM should be analyzed carefully to determine whether the thresholds subsequently can be increased further. International radiologic professional organizations, such as the American College of Radiology, should revisit the basis of their practice guidelines to reduce their implications about the danger of CIN with CE CT.
- SourceAvailable from: Wael Shabana
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- "Thus, none of the above meta-analyses have examined the causal effect of IV contrast material exposure on CI-AKI, while debates and differences of opinions exist on the nephrotoxic potential of contrast material when administered by IV route [36-39]. Moreover, in certain clinical setting (i.e. "
ABSTRACT: Background: Contrast-induced acute kidney injury is a common cause of iatrogenic acute kidney injury (AKI). Most of the published estimates of AKI after contrast use originate from the cardiac catheterization literature despite contrast-enhanced computed tomography (CT) scans being the more common setting for contrast use. This systematic review aims to summarize the current evidence about (1)the risk of AKI following intravenous (IV) contrast-enhanced CT scans and(2) the risk of clinical outcomes (i.e. death, hospitalization and need for renal replacement therapy) due to IV contrast-enhanced CT scans. Methods/design: A systematic literature search for published studies will be performed using MEDLINE, EMBASE and The COCHRANE Library databases. Unpublished studies will be identified by searching through grey literature. No language restriction will be applied.The review will consider all studies that have examined the association between IV contrast media and AKI. To be selected, the study should include two arms: one group of exposed patients who received IV contrast material before CT scans and one group of unexposed group who did not receive contrast material before CT scans. Two authors will independently screen titles and abstracts obtained from electronic databases, extract data and will assess the quality of the studies selected using the Cochrane's 'Risk of Bias' assessment tool for randomized trials and the Newcastle-Ottawa Scale for observational studies. A random-effects meta-analysis will be performed if there is no remarkable heterogeneity between studies. Discussion: This systematic review will provide synthesis of current evidence around the effect of IV contrast material on AKI and other clinical outcomes. Results will be helpful for making evidence-based recommendations and guidelines for clinical and radiologic settings. Systematic review registration: PROSPERO CRD42013003799.Systematic Reviews 08/2014; 3(1):94. DOI:10.1186/2046-4053-3-94
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- "Indeed, fear of CI-AKI is one of the most frequent reasons why CM is withheld from patients undergoing computed tomography (CT) and thus frequently compromises the diagnostic information gained from CT . This traditional concept has been challenged recently, in particular for intravenous administration of contrast material . This paradigm shift began when studies demonstrated a high rate of fluctuation in kidney function in patients without exposure to iodinated contrast material  , indicating that the existing observational studies on CI-AKI without a nonexposed control group are fundamentally flawed and likely to greatly overestimate the incidence of CI-AKI. "
ABSTRACT: Contrast-induced acute kidney injury (CI-AKI) is commonly defined as a decline in kidney function occurring in a narrow time window after administration of iodinated contrast material. The incidence of AKI after contrast material administration greatly depends on the specific definition and cutoff values used. Although self-limiting in most cases, postcontrast AKI carries a risk of more permanent renal insufficiency, dialysis, and death. The risk of AKI from contrast material, in particular when administered intravenously for contrast-enhanced CT, has been exaggerated by older, noncontrolled studies due to background fluctuations in renal function. More recent evidence from controlled studies suggests that the risk is likely nonexistent in patients with normal renal function, but there may be a risk in patients with renal insufficiency. However, even in this patient population, the risk of CI-AKI is probably much smaller than traditionally assumed. Since volume expansion is the only preventive strategy with a convincing evidence base, liberal hydration should be encouraged to further minimize the risk. The benefits of the diagnostic information gained from contrast-enhanced examinations will still need to be balanced with the potential risk of CI-AKI for the individual patient and clinical scenario.03/2014; 2014(2, article r31):859328. DOI:10.1155/2014/859328
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- "Due to the exponential relationship between SCrea and GFR, SCrea is very insensitive in patients with preexisting normal GFR [3, 7, 10, 12]. Day-to-day variations in SCrea observed in patients in whom no cause for rapid GFR changes could be identified indicate that SCrea is also insensitive at reduced preexisting GFR [13, 14]. Moreover, due to the kinetics of creatinine distribution among the body fluid compartments, SCrea is notoriously insensitive to rapid GFR changes such as the immediate GFR drop induced by CM: creatinine accumulation may take days, before SCrea increase fulfils diagnostic criteria [7, 10–12, 15, 16]. "
ABSTRACT: Iodinated contrast media (CM) can induce acute kidney injury (AKI). CM share common iodine-related cytotoxic features but differ considerably with regard to osmolality and viscosity. Meta-analyses of clinical trials generally failed to reveal renal safety differences of modern CM with regard to these physicochemical properties. While most trials' reliance on serum creatinine as outcome measure contributes to this lack of clinical evidence, it largely relies on the nature of prospective clinical trials: effective prophylaxis by ample hydration must be employed. In everyday life, patients are often not well hydrated; here we lack clinical data. However, preclinical studies that directly measured glomerular filtration rate, intrarenal perfusion and oxygenation, and various markers of AKI have shown that the viscosity of CM is of vast importance. In the renal tubules, CM become enriched, as water is reabsorbed, but CM are not. In consequence, tubular fluid viscosity increases exponentially. This hinders glomerular filtration and tubular flow and, thereby, prolongs intrarenal retention of cytotoxic CM. Renal cells become injured, which triggers hypoperfusion and hypoxia, finally leading to AKI. Comparisons between modern CM reveal that moderately elevated osmolality has a renoprotective effect, in particular, in the dehydrated state, because it prevents excessive tubular fluid viscosity.02/2014; 2014(1):358136. DOI:10.1155/2014/358136