Risk Score for Prediction of Contrast-Associated Acute Kidney Injury After PCI
abstract
This abstract is available on the publisher's site.
Access this abstract now Full Text Available for ClinicalKey SubscribersBACKGROUND
Contrast-associated acute kidney injury can occur after percutaneous coronary intervention (PCI). Prediction of the contrast-associated acute kidney injury risk is important for a tailored prevention and mitigation strategy. We sought to develop a simple risk score to estimate contrast-associated acute kidney injury risk based on a large contemporary PCI cohort.
METHODS
Consecutive patients undergoing PCI at a large tertiary care centre between Jan 1, 2012, and Dec 31, 2020, with available creatinine measurements both before and within 48 h after the procedure, were included; only patients on chronic dialysis were excluded. Patients treated between 2012 and 2017 comprised the derivation cohort and those treated between 2018 and 2020 formed the validation cohort. The primary endpoint was contrast-associated acute kidney injury, defined according to the Acute Kidney Injury Network. Independent predictors of contrast-associated acute kidney injury were derived from multivariate logistic regression analysis. Model 1 included only pre-procedural variables, whereas Model 2 also included procedural variables. A weighted integer score based on the effect estimate of each independent variable was used to calculate the final risk score for each patient. The impact of contrast-associated acute kidney injury on 1-year deaths was also evaluated.
FINDINGS
32 378 PCI procedures were performed and screened for inclusion in the present analysis. After the exclusion of patients without paired creatinine measurements, patients on chronic dialysis, and multiple procedures, 14 616 patients were included in the derivation cohort (mean age 66·2 years, 29·2% female) and 5606 were included in the validation cohort (mean age 67·0 years, 26·4% female). Contrast-associated acute kidney injury occurred in 860 (4·3%) patients. Independent predictors of contrast-associated acute kidney injury included in Model 1 were: clinical presentation, estimated glomerular filtration rate, left ventricular ejection fraction, diabetes, haemoglobin, basal glucose, congestive heart failure, and age. Additional independent predictors in Model 2 were: contrast volume, peri-procedural bleeding, no flow or slow flow post procedure, and complex PCI anatomy. The occurrence of contrast-associated acute kidney injury in the derivation cohort increased gradually from the lowest to the highest of the four risk score groups in both models (2·3% to 34·9% in Model 1, and 2·0% to 38·8% in Model 2). Inclusion of procedural variables in the model only slightly improved the discrimination of the risk score (C-statistic in the derivation cohort: 0·72 for Model 1 and 0·74 for model 2; in the validation cohort: 0·84 for Model 1 and 0·86 for Model 2). The risk of 1-year deaths significantly increased in patients with contrast-associated acute kidney injury (10·2% vs 2·5%; adjusted hazard ratio 1·76, 95% CI 1·31-2·36; p=0·0002), which was mainly due to excess 30-day deaths.
INTERPRETATION
A contemporary simple risk score based on readily available variables from patients undergoing PCI can accurately discriminate the risk of contrast-associated acute kidney injury, the occurrence of which is strongly associated with subsequent death.
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Additional Info
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A contemporary simple risk score for prediction of contrast-associated acute kidney injury after percutaneous coronary intervention: derivation and validation from an observational registry
Lancet 2021 Nov 12;[EPub Ahead of Print], R Mehran, R Owen, M Chiarito, U Baber, S Sartori, D Cao, J Nicolas, CA Pivato, M Nardin, P Krishnan, A Kini, S Sharma, S Pocock, G DangasFrom MEDLINE®/PubMed®, a database of the U.S. National Library of Medicine.
Acute kidney injury (AKI) is a known potential complication of intra-arterial contrast media administration and is often referred to as contrast-associated AKI (CA-AKI). Although severe, long-term renal impairment following percutaneous coronary intervention (PCI) is uncommon, its clinical implications are substantial. CA-AKI has heightened incidence after PCI in patients with pre-existing kidney disease, diabetes, hemodynamic compromise, acute coronary syndromes, and other patient-level and procedural characteristics that have been described in various CA-AKI risk scores.
Dr. Mehran and colleagues have now provided an updated version of their 2004 CA-AKI risk score. Using data from a single medical center, the authors reviewed all PCIs performed from 2012 through 2020 and included those where both a pre-PCI creatinine level and a post-PCI creatinine level (within 48 hours after PCI) were available, the patient did not have pre-existing end-stage renal disease on dialysis, and multiple procedures were not performed. Out of 32,378 PCIs during this time period, 14,616 were included in a derivation cohort and 5606 in a validation cohort. The occurrence of CA-AKI was defined using the Acute Kidney Injury Network (AKIN) criterion of an increase in serum creatinine of at least 50% or 0.3 mg/dL within 48 hours after PCI. Two multivariable models for predicting CA-AKI were generated: Model 1, which included only variables available pre-PCI; and Model 2, which also included procedural variables such as contrast volume and coronary anatomical complexity.
The incidence of CA-AKI was overall low, occurring in 4.3% of total patients. Both multivariable models showed graded relationships with CA-AKI occurrence. Model 1, which included clinical presentation, eGFR, left ventricular ejection fraction <40%, diabetes (± insulin), hemoglobin <11 g/dL, glucose level >150 mg/dL, congestive heart failure, and age >75 years, had a C-statistic of 0.72 in the derivation cohort (0.84 in the validation cohort). Patients were categorized into low, moderate, high, or very high risk based on an integer score with 1 point applied to each variable in the model. Rates of CA-AKI ranged from <5% in the roughly half of patients in the “low-risk” group to nearly 40% in the 1.6% of patients in the “very high–risk” group. Model 2, which included contrast volume, periprocedural bleeding, no/slow reflow, and complex coronary anatomy in addition to Model 1’s clinical variables, yielded overall similar findings, with a C-statistic of 0.74 in the derivation cohort (0.86 in the validation cohort). There was an association between CA-AKI occurrence and death at 1 year after multivariable adjustment.
So, where do these findings leave us? Foremost, these analyses reinforce prior observations that CA-AKI after PCI is uncommon overall, but is quite frequent in a small, identifiable subset of patients. It would be interesting to know how many of the patients meeting CA-AKI criteria went on to have longer-term renal impairment, but this information is not available in this data set. The association with subsequent mortality is, of course, confounded, and contributions from underlying patient characteristics versus occurrence of the AKI per se cannot be disentangled. One of the central challenges in applying this risk score is the absence of any interventions that substantially modify the risk of CA-AKI. Nonetheless, prediction scores such as Mehran 2 CA-AKI can importantly inform clinical risk/benefit discussion, risk adjustment in other analyses, and patient selection for studies of interventions intended to reduce CA-AKI incidence.