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

Abstract

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.

Keywords: contrast media; contrast‐induced nephropathy; myocardial infarction; primary percutaneous coronary intervention.

Figure 1

Comparison of areas under the receiver operator characteristic curves that relate various contrast media indices to the development of acute kidney injury. CrCl indicates creatinine clearance; eGFR, estimated glomerular filtration rate; Vol, volume.

Figure 2

ROC curves of the simplified scoring model for acute kidney injury in the primary percutaneous coronary intervention (PCI) and thrombolysis/no reperfusion groups.

Figure 3

A, Covariable balance before (red triangles) and after (blue squares) matching. The standardized difference after propensity matching (blue squares) are all well within 10%. B, Mirrored histogram of distribution of propensity scores for primary percutaneous coronary intervention (pPCI; bars above the zero line) vs no‐pPCI (bars below the zero line). ACE indicates angiotensin‐converting enzyme; ARB, angiotensin receptor blocker; GFR, glomerular filtration rate; Hb, hemoglobin; IABP, intra‐aortic balloon pump; LVEF, left ventricular ejection fraction.

Figure 4

Fitted mean multivariate‐adjusted trajectories of serum creatinine change over time in the primary percutaneous coronary intervention (pPCI) and thrombolysis/no reperfusion groups, based on the results from linear mixed models. The slops of the lines were similar (P=0.97 for interaction).

Figure 5

Cumulative incidence of mortality, readmission for heart failure, and recurrent myocardial infarction, according primary percutaneous coronary intervention (pPCI) treatment and occurrence of acute kidney injury (AKI).