Reviews in Cardiovascular Medicine  2020, Vol. 21 Issue (1): 9-23     DOI: 10.31083/j.rcm.2020.01.44 Contrast induced acute kidney injury in interventional cardiology: an update and key guidance for clinicians Federico Ronco1, Giuseppe Tarantini2, Peter A. McCullough3, *() 1 Emodinamica, Dipartimento Cardio-Toraco-Vascolare, Ospedale dell'Angelo, AULSS3 Serenissima, Mestre – Venezia 30174, Italy
2 Dipartimento di Scienze Cardiologiche, Toraciche e Vascolari, Policlinico Universitario di Padova, Centro Gallucci, Padova 35122, Italy
3 Baylor University Medical Center, Baylor Heart and Vascular Hospital, Baylor Heart and Vascular Institute, Dallas, Texas 75226, USA Abstract:

Contrast-induced acute kidney injury (CI-AKI) is a serious complication that can affect outcome and prognosis of patients undergoing percutaneous diagnostic and interventional procedures in catheterization laboratories. There have been advancements in case definition and epidemiology. Additionally strategies have emerged that are positioned to have impact in the catheterization laboratory for patients undergoing cardiovascular procedures. The aim of this review is to provide the state-of-the-art of diagnosis, prevention and management of CI-AKI in interventional cardiology.

Submitted:  25 March 2020      Accepted:  29 March 2020      Published:  30 March 2020      *Corresponding Author(s):  Peter A. McCullough     E-mail:  peteramccullough@gmail.com Service E-mail this article Add to citation manager E-mail Alert RSS Articles by authors Federico Ronco    Giuseppe Tarantini    Peter A. McCullough   

Figure 1.  Incidence of contrast-induced acute kidney injury (CI-AKI) and new end-stage renal disease requiring dialysis (ESRD) from the ACC Cath-PCI registry, reproduced with permission (McCullough et al., 2016).

Figure 2.  Anatomy of a single nephron and location of novel and conventional biomarkers of renal filtration and tubular epithelial cell damage, NGAL = neutrophil gelatinase associated lipocalin, L-FABP = L-type fatty-acid binding protein. Markers of filtration indicate transient reductions in glomerular function while cell damage markers indicate cellular injury, and the two together have a poorer prognosis than either alone. Not all of these markers have been validated for contrast-induced AKI.

Figure 3.  Pathogenesis of contrast-induced acute kidney injury.

Figure 4.  Algorithm for the prevention and management of contrast-induced acute kidney injury, ALARA = as low as reasonably achievable, Cr = serum creatinine, CI-AKI = contrast-induced acute kidney injury, eGFR = estimated glomerular filtration rate, NGAL = neutrophil associated lipocalin, L-FABP = L-type fatty-acid binding protein, TIMP2*IGFBP-7 = tissue inhibitor of metalloproteinase-2 concentration multiplied by insulin like growth factor binding protein-7 concentration, NSAIDS=nonsteroidal anti-inflammatory agents, ACS = acute coronary syndromes, CKD = chronic kidney disease, DM = diabetes mellitus, HF = heart failure, TAVI = transcatheter aortic valve insertion, RASi = renin angiotensin system inhibitors, LVEDP = left ventricular end-diastolic pressure.

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