Valentina Pistolesi1, Giuseppe Regolisti2, Santo Morabito3, Ilaria Gandolfini2, Silvia Corrado2, Giovanni Piotti2, Enrico Fiaccadori2. 1. Hemodialysis Unit, Policlinico Umberto I, "Sapienza" University, Viale del Policlinico, 155, 00161, Rome, Italy. valentina.pistolesi@uniroma1.it. 2. Acute and Chronic Renal Failure Unit, Parma University Medical School, Parma, Italy. 3. Hemodialysis Unit, Policlinico Umberto I, "Sapienza" University, Viale del Policlinico, 155, 00161, Rome, Italy.
Abstract
BACKGROUND AND AIMS: Contrast-induced acute kidney injury (CI-AKI) is the third leading cause of hospital-acquired acute kidney injury. It is more commonly observed following intra-arterial administration of iodinated contrast media (CM) for cardiac procedures in patients with pre-existing chronic kidney disease (CKD), and is associated with increased short- and long-term morbidity and mortality. This review investigates the key current evidence on CI-AKI definition, epidemiology and pathogenesis, as a basis for recommending preventive measures that can be implemented in clinical practice. METHODS: An extensive literature search was performed to identify the relevant studies describing the epidemiology, pathogenesis, outcome and prevention of CI-AKI. RESULTS AND CONCLUSION: Pre-existing CKD, intra-arterial administration and CM volume are the most important risk factors for CI-AKI. Since risk factors for CI-AKI are well defined, and the timing of renal insult is known, patients should be carefully stratified before the administration of CM, in order to reduce the negative impact of modifiable risk factors on renal function. The intravenous administration of moderate amounts of isotonic saline solution or bicarbonate solution still represents the principal intervention with documented and acceptable effectiveness for CI-AKI prevention. More data are needed on aggressive volume expansion strategies along with diuretics, targeting forced diuresis with high urinary output. The role of antioxidant agents remains controversial, and only moderate evidence exists in favour of N-acetylcysteine. Statins could contribute to reducing the incidence of CI-AKI, although their mechanism of action is not fully ascertained. No robust data demonstrate a reduction of CI-AKI incidence by peri-procedural hemodialysis/hemofiltration; renal replacement therapies may carry instead unnecessary risks. Remote ischemic preconditioning might represent a simple, non-invasive and cost effective preventive measure for CI-AKI prevention, but few data are currently available about its clinical application in patients at high risk of CI-AKI.
BACKGROUND AND AIMS: Contrast-induced acute kidney injury (CI-AKI) is the third leading cause of hospital-acquired acute kidney injury. It is more commonly observed following intra-arterial administration of iodinated contrast media (CM) for cardiac procedures in patients with pre-existing chronic kidney disease (CKD), and is associated with increased short- and long-term morbidity and mortality. This review investigates the key current evidence on CI-AKI definition, epidemiology and pathogenesis, as a basis for recommending preventive measures that can be implemented in clinical practice. METHODS: An extensive literature search was performed to identify the relevant studies describing the epidemiology, pathogenesis, outcome and prevention of CI-AKI. RESULTS AND CONCLUSION: Pre-existing CKD, intra-arterial administration and CM volume are the most important risk factors for CI-AKI. Since risk factors for CI-AKI are well defined, and the timing of renal insult is known, patients should be carefully stratified before the administration of CM, in order to reduce the negative impact of modifiable risk factors on renal function. The intravenous administration of moderate amounts of isotonic saline solution or bicarbonate solution still represents the principal intervention with documented and acceptable effectiveness for CI-AKI prevention. More data are needed on aggressive volume expansion strategies along with diuretics, targeting forced diuresis with high urinary output. The role of antioxidant agents remains controversial, and only moderate evidence exists in favour of N-acetylcysteine. Statins could contribute to reducing the incidence of CI-AKI, although their mechanism of action is not fully ascertained. No robust data demonstrate a reduction of CI-AKI incidence by peri-procedural hemodialysis/hemofiltration; renal replacement therapies may carry instead unnecessary risks. Remote ischemic preconditioning might represent a simple, non-invasive and cost effective preventive measure for CI-AKI prevention, but few data are currently available about its clinical application in patients at high risk of CI-AKI.
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