Contrast-induced acute kidney injury: the dark side of cardiac catheterization

Abstract

POLSKIE ARCHIWUM MEDYCYNY WEWNĘTRZNEJ 2015; 125 (12) 938the diagnostic criteria applied, comorbidities, and the type of procedure (coronary angiography [CA]; percutaneous coronary intervention [PCI]). CI-AKI is a challenge mainly for well-developed countries, in which excessive amounts of CM are used on a daily basis. When using the definition of CI-AKI as an increase of serum creatinine concentrations (SCr) by more than 25% relative to baseline and/or by more than 0.5 mg/dl at 48 hours after PCI, the rate of CI-AKI ranged from 3.3% according to the Mayo Clinic PCI registry 6 to 13.1% as stated by Mehran et al. 7 In the largest registry by Gurm et al, 8 based on 68 573 procedures, the rate of CI-AKI was 2.5%, defined as an absolute elevation in SCr by more than 0.5 mg/dl. Still, when only clinically relevant CI-AKI requiring dialysis was considered, the incidence decreased to a range from 0.8% to 1.7%. 9 This review sought to summarize the contemporary knowledge on pathophysiology, risk factors, diagnostic markers, and management of CI-AKI, with a special interest in CI-AKI as a result of cardiac catheterization. Accordingly, the Medline and EmBase databases were queried to Introduction Contrast-induced acute kidney injury (CI-AKI), previously known as contrast--induced nephropathy (CIN), represents a specific form of acute renal function impairment triggered by the use of iodinated contrast media (CM). As CI-AKI remains the subtype of acute kidney injury (AKI), it is recommended to use common definitions of AKI, such as the 2012 KDIGO criteria, 1 RIFLE classification (Risk, Injury, Failure, Loss of Function, End-Stage Renal Disease), 2 AKI Network criteria, 3 or the definition by Harjai 4 (Supplementary material online, Table S1).The rapid development of invasive cardiology triggered a massive increase in CM exposure. Since the implementation of the first CM in the 1950s, CI-AKI has emerged as the third most common subtype of hospital-acquired renal failure (reaching 11% of all cases), after renal hypoperfusion (42%) and postoperative AKI.5 Nearly half of all cases of CI-AKI occur after invasive cardiac procedures owing to CM-related nephrotoxicity and frequently present hemodynamic instability. 5The exact rate of CI-AKI in the setting of a cardiology department varies depending on ABSTRACTThe rapidly growing number of percutaneous coronary interventions has led to a considerable improvement in the outcome of patients with acute coronary syndromes, yet concurrently exposing patients to enormous volumes of contrast media with the inherent risk of renal function impairment. The issue of contrast-induced acute kidney injury (CI-AKI) is not only associated with direct sequelae such as prolonged hospital stay, but also with increased risk of chronic kidney disease, recurrent acute coronary syndromes, cerebral ischemia, and increased mortality rate. The ubiquitous application of contrast media warrants active search for reliable risk factors, diagnostic markers, preventive measures, and therapeutic modalities th...

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Relationship between Preoperative Urinary Microalbumin to Creatinine Ratio Level and Contrast-induced Nephropathy after Elective Coronary Angiography/Percutaneous Coronary Intervention

“…Contrast-induced nephropathy (CIN), known as contrast-induced acute kidney injury (CI-AKI), is a common complication after using contrast medium during coronary angiography (CAG), percutaneous coronary intervention (PCI) or other diagnostic and interventional therapy [1]. With an everincreasing number of patients receiving intravascular injection of iodinated contrast medium worldwide, CIN has gradually become the third leading cause of iatrogenic acute kidney injury, right after renal hypoperfusion and nephrotoxic drugs, accounts for about 11% [2,3]. The pathogenesis of CIN may include direct toxicity of contrast medium, renal medulla ischemia and hypoxia, oxidative stress, renal tubular obstruction, etc.…”