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

Abstract

BackgroundAcute 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 ResultsWe 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).ConclusionsThe 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.

Contrast-associated acute kidney injury is a myth: Yes

“…Further, a study performed in a large inpatient sample that controlled for comorbidity and acuity of illness found that patients with acute coronary syndromes (n = 1,251,812) who received CM experienced an unexpectedly lower rate of AKI as compared to patients who were not exposed to contrast (6.4% versus 17.4%) [10]. Finally, a propensity-matched cohort study of patients with non-STEMI reported one additional episode of AKI for every 62 participants treated with an early invasive approach instead of a conservative approach, with similar risks of dialysis or long-term risk of end-stage renal disease, but better long-term survival with the invasive approach [6] and in a propensitymatched cohort study of patients with STEMI, the risk of AKI was similar with and without CM exposure [7].…”

“…The prevailing belief that CM plays a central role in AKI has had major impacts over several decades, including promotion of potentially suboptimal clinical care at the patient level and subversion of a research agenda at the scientific level. Withholding CM on the basis of overestimated risk deprives individual patients of diagnostic studies and therapeutic interventions, many of which convey substantial proven benefit [6,7]. There are scenarios in which CM administration is unavoidable, however, and the perceived risk of CM administration associated with such scenarios has driven intense interest in preventive measures for CI-AKI.…”

“…The reported incidence of CI-AKI following percutaneous intervention (PCI) ranges from 1-2% in patients undergoing elective PCI to 10-20% in patients undergoing PCI for ST-elevation myocardial infarction (STEMI) [1,3,4,7]. While attributed to CM exposure, the marked increase in AKI rates in these patients more likely results from associated conditions including hypotension, hemodynamic instability/cardiogenic shock, acute heart failure, hemorrhage, and initiation of medications that alter renal hemodynamics (Fig.…”

“…1). Indeed, multiple retrospective controlled studies in patients undergoing PCI were unable to show a meaningful adverse effect of CM exposure [6,7,10]. Further, a study performed in a large inpatient sample that controlled for comorbidity and acuity of illness found that patients with acute coronary syndromes (n = 1,251,812) who received CM experienced an unexpectedly lower rate of AKI as compared to patients who were not exposed to contrast (6.4% versus 17.4%) [10].…”

Contrast-associated acute kidney injury is a myth: We are not sure

“…Caspi et al showed no difference in the AKI incidence between primary PCI (contrast group) and fibrinolysis or no reperfusion (no contrast group) in patients with ST-segment elevation myocardial infarction [12]. Wilhelm-Leen et al found a lower AKI incidence in patients receiving "any contrast. "…”