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

作者：Caspi Oren; Habib Manhal; Cohen Yuval; Kerner Arthur; Roguin Ariel; Abergel Eitan; Boulos Monther; Kapeliovich Michael R; Beyar Rafael; Nikolsky Eugenia; Aronson Doron

来源：Journal of the American Heart Association, 2017, 6(6): e005715.

DOI：10.1161/JAHA.117.005715

<jats:sec xml:lang="en">
<jats:title>Background</jats:title>
<jats:p xml:lang="en">
Acute kidney injury (
<jats:styled-content style="fixed-case">AKI</jats:styled-content>
) following primary percutaneous coronary intervention (
<jats:styled-content style="fixed-case">pPCI</jats:styled-content>
) is frequently interpreted as contrast‐induced
<jats:styled-content style="fixed-case">AKI</jats:styled-content>
but may result from other insults. We aimed to determine the causal association of contrast material exposure and the incidence of AKI following p
<jats:styled-content style="fixed-case">PCI</jats:styled-content>
using a control group of propensity score–matched patients with ST‐segment–elevation myocardial infarction who were not exposed to contrast material.
</jats:p>
</jats:sec>
<jats:sec xml:lang="en">
<jats:title>Methods and Results</jats:title>
<jats:p xml:lang="en">
We studied 2025 patients with ST‐segment–elevation myocardial infarction who underwent
<jats:styled-content style="fixed-case">pPCI</jats:styled-content>
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).
<jats:styled-content style="fixed-case">AKI</jats:styled-content>
was defined as creatinine of ≥0.5 mg/dL or &gt;25% rise within 72 hours.
<jats:styled-content style="fixed-case">AKI</jats:styled-content>
rates were similar in the
<jats:styled-content style="fixed-case">pPCI</jats:styled-content>
and control groups (10.3% versus 12.1%, respectively;
<jats:italic>P</jats:italic>
=0.38). Propensity score matching resulted in 931 matched pairs with
<jats:styled-content style="fixed-case">PCI</jats:styled-content>
and no
<jats:styled-content style="fixed-case">PCI,</jats:styled-content>
with balanced baseline covariates (standardized difference &lt;0.1). Among propensity score–matched patients,
<jats:styled-content style="fixed-case">AKI</jats:styled-content>
rates were not significantly different with and without
<jats:styled-content style="fixed-case">PCI</jats:styled-content>
(8.6% versus 10.9%,
<jats:italic>P</jats:italic>
=0.12). In the
<jats:styled-content style="fixed-case">pPCI</jats:styled-content>
cohort, independent predictors of
<jats:styled-content style="fixed-case">AKI</jats:styled-content>
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
<jats:styled-content style="fixed-case">PCI</jats:styled-content>
cohort had similar discriminatory capacity for
<jats:styled-content style="fixed-case">AKI</jats:styled-content>
in the control group (C statistic 0.81±0.02 and 0.78±0.02, respectively;
<jats:italic>P</jats:italic>
=0.26).
</jats:p>
</jats:sec>
<jats:sec xml:lang="en">
<jats:title>Conclusions</jats:title>
<jats:p xml:lang="en">
The development of
<jats:styled-content style="fixed-case">AKI</jats:styled-content>
in patients with ST‐segment–elevation myocardial infarction undergoing
<jats:styled-content style="fixed-case">pPCI</jats:styled-content>
is mainly related to older age, baseline estimated glomerular filtration rate, heart failure, and hemodynamic instability. Risk for
<jats:styled-content style="fixed-case">AKI</jats:styled-content>
is similar among ST‐segment–elevation myocardial infarction patients with and without contrast material exposure.
</jats:p>
</jats:sec>

• 出版日期2017-6