Prevention of Contrast-Induced Acute Kidney Injury: an Update

Chalikias, Georgios K.; Drosos, Ioannis; Tziakas, Dimitrios

doi:10.1007/s10557-016-6683-0

Cited by 42 publications

(34 citation statements)

References 78 publications

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“…These new variables could include circulating or urine biomarkers, systemic or kidney hemodynamics, and imaging markers. Neutrophil gelatinaseassociated lipocalin, interleukin-18, kidney injury molecule-1, L-fatty acid binding protein, and cystatin C are the most-known relevant biomarkers that have been used in AKI risk prediction [25][26][27]. Recent advances in methodologies to assess physiological biomarkers reflecting systemic or kidney hemodynamics were lately reviewed by the Acute Dialysis Quality Improvement (ADQI) workgroup [28].…”

Section: Discussionmentioning

confidence: 99%

Application of 17 Contrast-Induced Acute Kidney Injury Risk Prediction Models

et al. 2020

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Introduction: Contrast-induced acute kidney injury (CI-AKI) is a frequent complication of percutaneous coronary interventions (PCI). Various groups have developed and validated risk scores for CI-AKI. Although the majority of these risk scores achieve an adequate accuracy, their usability in clinical practice is limited and greatly debated. Objective: With the present study, we aimed to prospectively assess the diagnostic performance of recently published CI-AKI risk scores (up to 2018) in a cohort of patients undergoing PCI. Methods: We enrolled 1,247 consecutive patients (80% men, mean age 62 ± 10 years) treated with elective or urgent PCI. For each patient, we calculated the individual CI-AKI risk score based on 17 different risk models. CI-AKI was defined as an increase of ≥25% (liberal) or ≥0.5 mg/dL (strict) in pre-PCI serum creatinine 48 h after PCI. Results: CI-AKI definition and, therefore, CI-AKI incidence have a significant impact on risk model performance (median negative predictive value increased from 85 to 99%; median c-statistic increased from 0.516 to 0.603 using more strict definition criteria). All of the 17 published models were characterized by a weak-to-moderate discriminating ability mainly based on the identification of "true-negative" cases (median positive predictive value 19% with liberal criterion and 3% with strict criterion). In none of the models, c-statistic was > 0.800 with either CI-AKI definition. Novel, different combinations of the > 35 independent variables used in the published models either by down-or by up-scaling did not result in significant improvement in predictive performance. Conclusions: The predictive ability of all models was similar and only modest, derived mainly by identifying true-negative cases. A new approach is probably needed by adding novel markers or periprocedural characteristics.

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Section: Discussionmentioning

confidence: 99%

Application of 17 Contrast-Induced Acute Kidney Injury Risk Prediction Models

et al. 2020

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“…acute kidney injury (aKi) is a critical care syndrome in clinical practice, which is characterized by a rapid decline in renal function, and is responsible for high morbidity and mortality rates of patients in intensive care units (1). the clinical symptoms of aKi are caused by diverse components, including sepsis-induced infection (2), liver transplantation (3), cardiac surgery (4) and contrast media (5). lipopolysaccharide (lPS) is an endotoxin produced following infection by Gram negative bacteria, and remains the most common trigger for aKi (6).…”

Section: Introductionmentioning

confidence: 99%

Mechanism of long non-coding RNA MALAT1 in lipopolysaccharide-induced acute kidney injury is mediated by the miR-146a/NF-κB signaling pathway

et al. 2017

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The present study aimed to examine the expression and function of the metastasis-associated lung adenocarcinoma transcript 1 (MALAT1)/microRNA (miR)-146a/nuclear factor (NF)-κB axis in lipopolysaccharide (LPS)-induced acute kidney injury (AKI). The mRNA levels of MALAT1 and miR-146a in AKI tissues and cells were detected using reverse transcription-quantitative polymerase chain reaction analysis. The NF-κB pathway proteins and cell viability were assessed using western blot analysis and the MTT method, respectively. The secretion of inflammatory factors was determined using the ELISA method. The present study also examined effects of the abnormal expression of MALAT1 and miR-146a on cytokines and the NF-κB pathway. A potential binding region between MALAT1 and miR-146a was confirmed via RNA immunoprecipitation. The results revealed that the upregulation of MALAT1 reduced the expression of miR‑146a, and there was a negative linear correlation between MALAT1 and miR-146a in a RNA-induced silencing complex‑dependent manner. The expression levels of miR-146a were lower in the kidney injury specimens and NRK-52E cells, compared with those in the controls. MALAT1 knockdown and the overexpression of miR-146a reduced the production of phosphorylated inhibitor of NF-κB and np65 protein. miR‑146a was found to be transcriptionally induced by NF-κB, and miR-146a repressed the pro-inflammatory NF-κB pathway and downstream transcription factors. Taken together, these data indicated that the MALAT1/miR‑146a/NF-κB pathway exerted key functions in LPS-induced AKI, and provided novel insights into the mechanisms of this therapeutic candidate for the treatment of the disease.

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“…The limitations of our study mainly include: (1) This study is a single-center prospective observational study. In the process of inclusion, some patients were excluded due to incoordination with examination, which caused a selection bias.…”

Section: Discussionmentioning

confidence: 99%

“…With the rapid development and pervasive application of imaging diagnosis and treatment techniques such as contrast-enhanced CT, angiography and interventional therapy, the application of contrast medium is increasing in the clinic. Contrast-induced nephropathy (CIN), known as contrast-induced acute kidney injury (CI-AKI), is a common complication after using contrast medium during coronary angiography (CAG), percutaneous coronary intervention (PCI) or other diagnostic and interventional therapy [1]. With an everincreasing number of patients receiving intravascular injection of iodinated contrast medium worldwide, CIN has gradually become the third leading cause of iatrogenic acute kidney injury, right after renal hypoperfusion and nephrotoxic drugs, accounts for about 11% [2,3].…”

Section: Introductionmentioning

confidence: 99%

Relationship between Preoperative Urinary Microalbumin to Creatinine Ratio Level and Contrast-induced Nephropathy after Elective Coronary Angiography/Percutaneous Coronary Intervention

Ma¹,

Tang²,

Qin³

et al. 2018

Angiol

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Objective: To investigate the predictive value of preoperative urinary microalbumin to creatinine ratio (UACR) level for early diagnosis of contrast-induced nephropathy (CIN). Methods:A total of 180 patients scheduled to undergo elective coronary angiography (CAG)/percutaneous coronary intervention (PCI) in our department from November 2016 to September 2017 were selected into this prospective study. Patients were allocated to high UACR group (UACR ≥ 30, n=35) and control group (UACR<30, n=145) according to the UACR level. The patients were also divided into CIN group (n=32) and no CIN group (n=148). Multivariable logistic regression model was used to investigate the risk factors of CIN. This trial was registered on the Chinese Clinical Trial Registry on 23 May 2017 (Registration No. ChiCTR-OOC-17011467).Results: 32 patients developed CIN (17.78%). The incidence of CIN was significantly higher in high UACR group than in the control group (P0.001). The ratio of high UACR in CIN group was significantly higher than no CIN group (P0.001). Multivariable logistic regression analysis indicated that preoperative UACR level (P0.001, 95%CI: 3.81929.223, OR: 10.564) was an independent risk factor of CIN. Conclusion:Preoperative UACR level appears to be an independent predictive factor for early diagnosis of CIN.

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Prevention of Contrast-Induced Acute Kidney Injury: an Update

Cited by 42 publications

References 78 publications

Application of 17 Contrast-Induced Acute Kidney Injury Risk Prediction Models

Application of 17 Contrast-Induced Acute Kidney Injury Risk Prediction Models

Mechanism of long non-coding RNA MALAT1 in lipopolysaccharide-induced acute kidney injury is mediated by the miR-146a/NF-κB signaling pathway

Relationship between Preoperative Urinary Microalbumin to Creatinine Ratio Level and Contrast-induced Nephropathy after Elective Coronary Angiography/Percutaneous Coronary Intervention

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