Cargando…

Acute Kidney Injury After Primary Angioplasty: Is Contrast‐Induced Nephropathy the Culprit?

BACKGROUND: Acute kidney injury (AKI) following primary percutaneous coronary intervention (pPCI) is frequently interpreted as contrast‐induced AKI but may result from other insults. We aimed to determine the causal association of contrast material exposure and the incidence of AKI following pPCI us...

Descripción completa

Detalles Bibliográficos
Autores principales: Caspi, Oren, Habib, Manhal, Cohen, Yuval, Kerner, Arthur, Roguin, Ariel, Abergel, Eitan, Boulos, Monther, Kapeliovich, Michael R., Beyar, Rafael, Nikolsky, Eugenia, Aronson, Doron
Formato: Online Artículo Texto
Lenguaje:English
Publicado: John Wiley and Sons Inc. 2017
Materias:
Acceso en línea:https://www.ncbi.nlm.nih.gov/pmc/articles/PMC5669180/
https://www.ncbi.nlm.nih.gov/pubmed/28647690
http://dx.doi.org/10.1161/JAHA.117.005715
_version_ 1783275809811726336
author Caspi, Oren
Habib, Manhal
Cohen, Yuval
Kerner, Arthur
Roguin, Ariel
Abergel, Eitan
Boulos, Monther
Kapeliovich, Michael R.
Beyar, Rafael
Nikolsky, Eugenia
Aronson, Doron
author_facet Caspi, Oren
Habib, Manhal
Cohen, Yuval
Kerner, Arthur
Roguin, Ariel
Abergel, Eitan
Boulos, Monther
Kapeliovich, Michael R.
Beyar, Rafael
Nikolsky, Eugenia
Aronson, Doron
author_sort Caspi, Oren
collection PubMed
description BACKGROUND: Acute kidney injury (AKI) following primary percutaneous coronary intervention (pPCI) is frequently interpreted as contrast‐induced AKI but may result from other insults. We aimed to determine the causal association of contrast material exposure and the incidence of AKI following pPCI using a control group of propensity score–matched patients with ST‐segment–elevation myocardial infarction who were not exposed to contrast material. METHODS AND RESULTS: We studied 2025 patients with ST‐segment–elevation myocardial infarction who underwent pPCI and 1025 patients receiving fibrinolysis or no reperfusion who were not exposed to contrast material during the first 72 hours of hospital stay (control group). AKI was defined as creatinine of ≥0.5 mg/dL or >25% rise within 72 hours. AKI rates were similar in the pPCI and control groups (10.3% versus 12.1%, respectively; P=0.38). Propensity score matching resulted in 931 matched pairs with PCI and no PCI, with balanced baseline covariates (standardized difference <0.1). Among propensity score–matched patients, AKI rates were not significantly different with and without PCI (8.6% versus 10.9%, P=0.12). In the pPCI cohort, independent predictors of AKI included age ≥70 years, insulin‐treated diabetes mellitus, diuretic therapy, anterior infarction, baseline estimated glomerular filtration rate, and variables related to the presence of pump failure (higher Killip class, intra‐aortic balloon pump use) and reduced left ventricular ejection fraction but not contrast material dose. A risk score based on the PCI cohort had similar discriminatory capacity for AKI in the control group (C statistic 0.81±0.02 and 0.78±0.02, respectively; P=0.26). CONCLUSIONS: The development of AKI in patients with ST‐segment–elevation myocardial infarction undergoing pPCI is mainly related to older age, baseline estimated glomerular filtration rate, heart failure, and hemodynamic instability. Risk for AKI is similar among ST‐segment–elevation myocardial infarction patients with and without contrast material exposure.
format Online
Article
Text
id pubmed-5669180
institution National Center for Biotechnology Information
language English
publishDate 2017
publisher John Wiley and Sons Inc.
record_format MEDLINE/PubMed
spelling pubmed-56691802017-11-09 Acute Kidney Injury After Primary Angioplasty: Is Contrast‐Induced Nephropathy the Culprit? Caspi, Oren Habib, Manhal Cohen, Yuval Kerner, Arthur Roguin, Ariel Abergel, Eitan Boulos, Monther Kapeliovich, Michael R. Beyar, Rafael Nikolsky, Eugenia Aronson, Doron J Am Heart Assoc Original Research BACKGROUND: Acute kidney injury (AKI) following primary percutaneous coronary intervention (pPCI) is frequently interpreted as contrast‐induced AKI but may result from other insults. We aimed to determine the causal association of contrast material exposure and the incidence of AKI following pPCI using a control group of propensity score–matched patients with ST‐segment–elevation myocardial infarction who were not exposed to contrast material. METHODS AND RESULTS: We studied 2025 patients with ST‐segment–elevation myocardial infarction who underwent pPCI and 1025 patients receiving fibrinolysis or no reperfusion who were not exposed to contrast material during the first 72 hours of hospital stay (control group). AKI was defined as creatinine of ≥0.5 mg/dL or >25% rise within 72 hours. AKI rates were similar in the pPCI and control groups (10.3% versus 12.1%, respectively; P=0.38). Propensity score matching resulted in 931 matched pairs with PCI and no PCI, with balanced baseline covariates (standardized difference <0.1). Among propensity score–matched patients, AKI rates were not significantly different with and without PCI (8.6% versus 10.9%, P=0.12). In the pPCI cohort, independent predictors of AKI included age ≥70 years, insulin‐treated diabetes mellitus, diuretic therapy, anterior infarction, baseline estimated glomerular filtration rate, and variables related to the presence of pump failure (higher Killip class, intra‐aortic balloon pump use) and reduced left ventricular ejection fraction but not contrast material dose. A risk score based on the PCI cohort had similar discriminatory capacity for AKI in the control group (C statistic 0.81±0.02 and 0.78±0.02, respectively; P=0.26). CONCLUSIONS: The development of AKI in patients with ST‐segment–elevation myocardial infarction undergoing pPCI is mainly related to older age, baseline estimated glomerular filtration rate, heart failure, and hemodynamic instability. Risk for AKI is similar among ST‐segment–elevation myocardial infarction patients with and without contrast material exposure. John Wiley and Sons Inc. 2017-06-24 /pmc/articles/PMC5669180/ /pubmed/28647690 http://dx.doi.org/10.1161/JAHA.117.005715 Text en © 2017 The Authors. Published on behalf of the American Heart Association, Inc., by Wiley. This is an open access article under the terms of the Creative Commons Attribution‐NonCommercial (http://creativecommons.org/licenses/by-nc/4.0/) License, which permits use, distribution and reproduction in any medium, provided the original work is properly cited and is not used for commercial purposes.
spellingShingle Original Research
Caspi, Oren
Habib, Manhal
Cohen, Yuval
Kerner, Arthur
Roguin, Ariel
Abergel, Eitan
Boulos, Monther
Kapeliovich, Michael R.
Beyar, Rafael
Nikolsky, Eugenia
Aronson, Doron
Acute Kidney Injury After Primary Angioplasty: Is Contrast‐Induced Nephropathy the Culprit?
title Acute Kidney Injury After Primary Angioplasty: Is Contrast‐Induced Nephropathy the Culprit?
title_full Acute Kidney Injury After Primary Angioplasty: Is Contrast‐Induced Nephropathy the Culprit?
title_fullStr Acute Kidney Injury After Primary Angioplasty: Is Contrast‐Induced Nephropathy the Culprit?
title_full_unstemmed Acute Kidney Injury After Primary Angioplasty: Is Contrast‐Induced Nephropathy the Culprit?
title_short Acute Kidney Injury After Primary Angioplasty: Is Contrast‐Induced Nephropathy the Culprit?
title_sort acute kidney injury after primary angioplasty: is contrast‐induced nephropathy the culprit?
topic Original Research
url https://www.ncbi.nlm.nih.gov/pmc/articles/PMC5669180/
https://www.ncbi.nlm.nih.gov/pubmed/28647690
http://dx.doi.org/10.1161/JAHA.117.005715
work_keys_str_mv AT caspioren acutekidneyinjuryafterprimaryangioplastyiscontrastinducednephropathytheculprit
AT habibmanhal acutekidneyinjuryafterprimaryangioplastyiscontrastinducednephropathytheculprit
AT cohenyuval acutekidneyinjuryafterprimaryangioplastyiscontrastinducednephropathytheculprit
AT kernerarthur acutekidneyinjuryafterprimaryangioplastyiscontrastinducednephropathytheculprit
AT roguinariel acutekidneyinjuryafterprimaryangioplastyiscontrastinducednephropathytheculprit
AT abergeleitan acutekidneyinjuryafterprimaryangioplastyiscontrastinducednephropathytheculprit
AT boulosmonther acutekidneyinjuryafterprimaryangioplastyiscontrastinducednephropathytheculprit
AT kapeliovichmichaelr acutekidneyinjuryafterprimaryangioplastyiscontrastinducednephropathytheculprit
AT beyarrafael acutekidneyinjuryafterprimaryangioplastyiscontrastinducednephropathytheculprit
AT nikolskyeugenia acutekidneyinjuryafterprimaryangioplastyiscontrastinducednephropathytheculprit
AT aronsondoron acutekidneyinjuryafterprimaryangioplastyiscontrastinducednephropathytheculprit