Dataset Information

A circulating miRNA signature for early diagnosis of acute kidney injury following acute myocardial infarction.

ABSTRACT:

Background

Acute kidney injury (AKI) is a common complication of acute myocardial infarction (AMI), and is associated with adverse outcomes. The study aimed to identify a miRNA signature for the early diagnosis of post-AMI AKI.

Methods

A total of 108 patients admitted to a coronary care unit (CCU) were divided into four subgroups: AMI^-AKI^-, AMI⁺AKI^-, AMI⁺AKI⁺, and AMI^-AKI⁺. Thirty-six miRNA candidates were selected based on an extensive literature review. Real-time quantitative RT-PCR analysis was used to determine the expression levels of these miRNAs in the serum collected on the day of CCU admittance. TargetScan 7.1 and miRDB databases were used for target prediction and Metacore 6.13 was used for pathway analysis.

Results

Through a stepwise selection based on abundance, hemolytic effect and differential expression between four groups, 9 miRNAs were found to have significantly differential expression levels as potential biomarkers for post-AMI AKI specifically. Noticeably, the expression levels of miR-24, miR-23a and miR-145 were significantly down-regulated in AMI⁺AKI⁺ patients compared to those in AMI⁺AKI^- patients. Combination of the three miRNAs as a panel showed the best performance in the early detection of AKI following AMI (AUC?=?0.853, sensitivity 95.65%), compared to the analysis of serum neutrophil gelatinase-associated lipocalin (AUC?=?0.735, sensitivity 63.16%). Furthermore, bioinformatic analysis indicated that these three miRNAs regulate the transforming growth factor beta signaling pathway and involve in apoptosis and fibrosis in AKI.

Conclusions

For the first time, this study identify a unique circulating miRNA signature (miR-24-3p, miR-23a-3p, miR-145-5p) that can potentially early detect AKI following AMI and may be involved in renal injury and fibrosis in post-AMI AKI pathogenesis.

SUBMITTER: Fan PC

PROVIDER: S-EPMC6492315 | biostudies-literature | 2019 Apr

REPOSITORIES: biostudies-literature

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Publications

A circulating miRNA signature for early diagnosis of acute kidney injury following acute myocardial infarction.

Fan Pei-Chun PC Chen Chia-Chun CC Peng Chen-Ching CC Chang Chih-Hsiang CH Yang Chia-Hung CH Yang Chi C Chu Lichieh Julie LJ Chen Yung-Chang YC Yang Chih-Wei CW Chang Yu-Sun YS Chu Pao-Hsien PH

Journal of translational medicine 20190430 1

<h4>Background</h4>Acute kidney injury (AKI) is a common complication of acute myocardial infarction (AMI), and is associated with adverse outcomes. The study aimed to identify a miRNA signature for the early diagnosis of post-AMI AKI.<h4>Methods</h4>A total of 108 patients admitted to a coronary care unit (CCU) were divided into four subgroups: AMI<sup>-</sup>AKI<sup>-</sup>, AMI<sup>+</sup>AKI<sup>-</sup>, AMI<sup>+</sup>AKI<sup>+</sup>, and AMI<sup>-</sup>AKI<sup>+</sup>. Thirty-six miRNA can ...[more]

PMID: 31039814

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Project description:BackgroundPreclinical data suggest that an acute inflammatory response following myocardial infarction (MI) accelerates systemic atherosclerosis. Using combined positron emission and computed tomography, we investigated whether this phenomenon occurs in humans.Methods and resultsOverall, 40 patients with MI and 40 with stable angina underwent thoracic 18F-fluorodeoxyglucose combined positron emission and computed tomography scan. Radiotracer uptake was measured in aortic atheroma and nonvascular tissue (paraspinal muscle). In 1003 patients enrolled in the Global Registry of Acute Coronary Events, we assessed whether infarct size predicted early (≤30 days) and late (>30 days) recurrent coronary events. Compared with patients with stable angina, patients with MI had higher aortic 18F-fluorodeoxyglucose uptake (tissue-to-background ratio 2.15±0.30 versus 1.84±0.18, P<0.0001) and plasma C-reactive protein concentrations (6.50 [2.00 to 12.75] versus 2.00 [0.50 to 4.00] mg/dL, P=0.0005) despite having similar aortic (P=0.12) and less coronary (P=0.006) atherosclerotic burden and similar paraspinal muscular 18F-fluorodeoxyglucose uptake (P=0.52). Patients with ST-segment elevation MI had larger infarcts (peak plasma troponin 32 300 [10 200 to >50 000] versus 3800 [1000 to 9200] ng/L, P<0.0001) and greater aortic 18F-fluorodeoxyglucose uptake (2.24±0.32 versus 2.02±0.21, P=0.03) than those with non-ST-segment elevation MI. Peak plasma troponin concentrations correlated with aortic 18F-fluorodeoxyglucose uptake (r=0.43, P=0.01) and, on multivariate analysis, independently predicted early (tertile 3 versus tertile 1: relative risk 4.40 [95% CI 1.90 to 10.19], P=0.001), but not late, recurrent MI.ConclusionsThe presence and extent of MI is associated with increased aortic atherosclerotic inflammation and early recurrent MI. This finding supports the hypothesis that acute MI exacerbates systemic atherosclerotic inflammation and remote plaque destabilization: MI begets MI.Clinical trial registrationURL: https://www.clinicaltrials.gov. Unique identifier: NCT01749254.

Project description:BackgroundData on the association between obesity and acute kidney injury (AKI) in patients with ST-elevation myocardial infarction (STEMI) are sparse and inconclusive. We aimed to evaluate the association between obesity and AKI and the outcome in these patients.MethodsA retrospective observational study of 3979 STEMI patients undergoing percutaneous coronary intervention (PCI) was performed at a single center. Patients with and without AKI were compared. Patients were also divided into three categories according to BMI, and these were compared. All-cause mortality was determined at 30 days and over a median period of 7.0 years.ResultsThe incidence of AKI was similar in all BMI categories. There was no association between BMI categories and AKI (p = 0.089). The Spearman correlation coefficient between BMI categories and AKI showed no correlation (r = -0.005; p = 0.75). More AKI patients died within 30 days and in the long term [137 (18.5%) and 283 (38.1%) patients in the AKI group died compared to 118 (3.6%) and 767 (23.1%) in the non-AKI group; p < 0.0001]. AKI was harmful in all BMI categories (p < 0.0001) and was associated with more than a 2.5-fold and a 1.5-fold multivariable-adjusted 30-day and long-term mortality risk, respectively (aOR 2.59; 95% CI 1.84-3.64; p < 0.0001, aHR 1.54; 95% CI 1.32-1.80; p < 0.0001). BMI categories were not associated with 30-day mortality (p = 0.26) but were associated with long-term mortality (p < 0.0001). Overweight and obese patients had an approximately 25% lower long-term multivariable-adjusted risk of death than normal-weight patients. In patients with AKI, BMI was only associated with long-term risk (p = 0.022). Obesity had an additional beneficial effect in these patients, and only patients with obesity, but not overweight patients, had a lower multivariable adjusted long-term mortality risk than normal-weight patients (aHR 062; 95% CI 0.446-0.88 p = 0.007).ConclusionsIn patients who experienced AKI, obesity had an additional positive modifying effect. Our data suggest that the incidence of AKI in STEMI patients is not BMI-dependent.

Dataset Information

A circulating miRNA signature for early diagnosis of acute kidney injury following acute myocardial infarction.

Background

Methods

Results

Conclusions

Publications

A circulating miRNA signature for early diagnosis of acute kidney injury following acute myocardial infarction.

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