Contrast-induced nephropathy and oxidative stress: mechanistic insights for better interventional approaches
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(2020) 18:400 Kusirisin et al. J Transl Med https://doi.org/10.1186/s12967-020-02574-8
Open Access
REVIEW
Contrast‑induced nephropathy and oxidative stress: mechanistic insights for better interventional approaches Prit Kusirisin1,2,3, Siriporn C. Chattipakorn2,3 and Nipon Chattipakorn2,3,4*
Abstract Contrast-induced nephropathy (CIN) or contrast-induced acute kidney injury (CI-AKI) is an iatrogenic acute kidney injury observed after intravascular administration of contrast media for intravascular diagnostic procedures or therapeutic angiographic intervention. High risk patients including those with chronic kidney disease (CKD), diabetes mellitus with impaired renal function, congestive heart failure, intraarterial intervention, higher volume of contrast, volume depletion, old age, multiple myeloma, hypertension, and hyperuricemia had increased prevalence of CIN. Although CIN is reversible by itself, some patients suffer this condition without renal recovery leading to CKD or even endstage renal disease which required long term renal replacement therapy. In addition, both CIN and CKD have been associated with increasing of mortality. Three pathophysiological mechanisms have been proposed including direct tubular toxicity, intrarenal vasoconstriction, and excessive production of reactive oxygen species (ROS), all of which lead to impaired renal function. Reports from basic and clinical studies showing potential preventive strategies for CIN pathophysiology including low- or iso-osmolar contrast media are summarized and discussed. In addition, reports on pharmacological interventions to reduce ROS and attenuate CIN are summarized, highlighting potential for use in clinical practice. Understanding this contributory mechanism could pave ways to improve therapeutic strategies in combating CIN. Keyword: Contrast-induced nephropathy, Oxidative stress, Mitochondria, Prevention, Statin Introduction Contrast-induced nephropathy (CIN) or contrastinduced acute kidney injury (CI-AKI) is an iatrogenic acute kidney injury (AKI) observed after intravascular administration of contrast media (CM) for diagnostic procedures or therapeutic angiographic interventions [1–4]. Chemical hypersensitivity has also been reported as another side effect of CM [5]. According to the Kidney Disease Improving Global Outcomes (KDIGO) clinical practice guidelines for AKI, a serum creatinine (Cr)
*Correspondence: [email protected] 2 Cardiac Electrophysiology Research and Training Center, Faculty of Medicine, Chiang Mai University, Chiang Mai, Thailand Full list of author information is available at the end of the article
increase of at least 0.3 mg/dL (or 26.5 µmol/L) over the baseline value within 48 h after exposure to CM, or an increase greater than 1.5 times over the baseline value within 7 days after exposure to CM, or a urinary volume of less than 0.5 mL/kg/h for at least 6 h after exposure, are the definition of this condition [6]. Incidence of CIN has been reported in 1–25% of cases of hospital-acquired AKI, and is the third comm
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