Strategies to Reduce the Risk of Contrast-Induced Nephropathy

Stacul, Fulvio; Adam, Andy; Becker, Christoph R.; Davidson, Charles J.; Lameire, Norbert; McCullough, Peter A.; Tumlin, James A.

doi:10.1016/j.amjcard.2006.01.024

Cited by 213 publications

(194 citation statements)

References 103 publications

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“…After careful revision of available information from performed studies, they suggest adequate intravenous volume expansion with isotonic crystalloid (1.0-1.5 mL/kg/hr) for 3 to 12 hr before the procedure and continued for 6 to 24 hr to prevent development of CIN in patients at risk [57]. Caution is needed in patients with chronic heart failure.…”

Section: Hydrationmentioning

confidence: 99%

Contrast‐induced nephropathy

Pučelíková

Dangas

Mehran

2007

Cathet Cardio Intervent

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Contrast induced nephropathy (CIN) is an iatrogenic disorder, resulting from exposure to contrast media. Contrast-induced hemodynamic and direct cytotoxic effects on renal structures are highly evident in its pathogenesis, whereas other mechanisms are still poorly understood. CIN is typically defined as an increase in serum creatinine by either 0.5 mg/dl or by 25% from baseline within the first 2-3 days after contrast administration. Although rare in the general population, CIN has a high incidence in patients with an underlying renal disorder, in diabetics, and the elderly. The risk factors are synergistic in their ability to produce CIN. The best way to prevent CIN is to identify the patients at risk and to provide adequate peri-procedural hydration. The role of various drugs in prevention of CIN is still controversial and warrants future studies. Despite remaining uncertainty regarding the degree of nephrotoxicity produced by various contrast agents, in current practice non-ionic low-osmolar contrast media are preferred over the high-osmolar contrast media in patients with renal impairment.

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Section: Hydrationmentioning

confidence: 99%

Contrast‐induced nephropathy

Pučelíková

Dangas

Mehran

2007

Cathet Cardio Intervent

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“…Extracellular volume expansion plays a well-established role in reducing the risk of contrastinduced AKI, although few trials have directly addressed the ideal protocol. 43 Intravenous volume expansion before and after administration of contrast medium appears to be more effective than either bolus volume expansion during the procedure 44 or removal of restrictions on oral fluid intake. 45 Isotonic saline has been found to be better than 0.45% saline and is given intravenously before and after administration of contrast medium for a total of 24 hours.…”

Section: Minimizing Riskmentioning

confidence: 99%

Contrast-Induced Acute Kidney Injury: Specialty-Specific Protocols for Interventional Radiology, Diagnostic Computed Tomography Radiology, and Interventional Cardiology

Goldfarb

McCullough

McDermott

et al. 2009

Mayo Clinic Proceedings

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135

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Contrast-induced acute kidney injury (AKI) (also known as contrast-induced nephropathy) is an abrupt deterioration in renal function that can be associated with use of iodinated contrast medium. Although the increase in serum creatinine concentration is transient in most cases, contrast-induced AKI may lead to increased morbidity and mortality rates in selected at-risk populations. This review summarizes the findings of a multidisciplinary panel composed of computed tomography radiologists, interventional radiologists, cardiologists, and nephrologists convened to address the specialty-specific issues associated with minimizing the incidence of contrast-induced AKI. As part of this initiative, the panel developed specialty-specific protocols for preventing contrast-induced AKI, taking into account, for example, the variations in patient risk profile, inpatient or outpatient status, and staffing resources that characterize various clinical settings. The 3 protocols, each reflecting a consensus of expert opinion, address the prevention of contrast-induced AKI in interventional radiology, diagnostic computed tomography radiology, and interventional cardiology settings. The protocols are presented in the context of a review of recent guidelines and published reports of trials that discuss contrast-induced AKI and its prevention. © 2009 Mayo Foundation for Medical Education and ResearchA cute kidney injury (AKI) is a heterogeneous disorder with multiple etiologies, risk factors, and clinical presentations. Although patients with AKI are ultimately cared for by nephrologists, AKI occurs in various clinical settings and is associated with a specific etiology in each. The term contrast-induced AKI refers to the disorder as it occurs after exposure to iodinated contrast media, a disorder that has been more commonly known as contrastinduced nephropathy (CIN). The Acute Kidney Injury Network, recognizing the need for improving outcomes associated with the various forms of AKI, recently proposed using the following standardized diagnostic definition in all cases: an abrupt (within 48 hours) reduction in kidney function, evidenced by an increase in the serum creatinine concentration of at least 0.3 mg/dL (to convert to µmol/L, multiply by 88.4) or at least 50% from baseline or a reduction in urine output (documented oliguria of <0.5 mL/kg/h for >6 hours).1,2 The criterion of oliguria does not apply for many cases of contrast-induced AKI because patients are treated with intravenous fluids before and after the procedure with the goal of increasing periprocedural urine output. The most commonly used definition of CIN is an increase from the baseline serum creatinine concentration of at least 0.5 mg/dL or at least 25% within 48 to 72 hours after exposure to contrast media. [3][4][5] Because the medical community is moving to adopt the concept and terminology of the American College of Radiology (ACR) in reference to studies of contrast-induced renal dysfunction and its prevention, 6 this report will do the same. However, we rec...

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“…2,3 Volume expansion with saline is the standard preventive strategy of CIN. 4,5 Because of its antioxidant and vasodilatatory properties, N-acetylcysteine (NAC) has been proposed for the prevention of CIN. 6 More recently it has been suggested that hydration with sodium bicarbonate (SB) might reduce the incidence of CIN.…”

Section: Introductionmentioning

confidence: 99%

Prevention of Contrast‐induced Nephropathy: A Single Center Randomized Study

Castini

Lucreziotti

Bosotti

et al. 2010

Clinical Cardiology

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Background: Contrast-induced nephropathy (CIN) is the third cause of acute deterioration of renal function in hospitalized patients. Hypothesis: The purpose of the study was to compare the efficacy of saline infusion, saline infusion plus N-acetylcysteine (NAC), and sodium bicarbonate (SB) infusion to prevent CIN in patients undergoing coronary angiography and/or percutaneous coronary intervention. Methods: We prospectively studied 156 patients with a baseline creatinine level ≥1.2 mg/dL. The primary endpoint was the development of CIN, defined as an increase in serum creatinine concentration ≥25% over the baseline value within 5 days from contrast exposure. Results: Contrast-induced nephropathy developed in 23 patients (14.7%). Incidence of the primary endpoint was similar in the 3 groups of treatment, occurring in 7 patients (14%) in the saline infusion group, in 9 (17%) in the saline infusion plus NAC group, and in 7 (14%) in the SB infusion group. Conclusions: Our findings suggest that neither the addition of NAC nor the administration of SB add further benefit in CIN prevention, compared to standard hydration with isotonic saline infusion.

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Strategies to Reduce the Risk of Contrast-Induced Nephropathy

Cited by 213 publications

References 103 publications

Contrast‐induced nephropathy

Contrast‐induced nephropathy

Contrast-Induced Acute Kidney Injury: Specialty-Specific Protocols for Interventional Radiology, Diagnostic Computed Tomography Radiology, and Interventional Cardiology

Prevention of Contrast‐induced Nephropathy: A Single Center Randomized Study

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