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      IL-10 Combined with NGAL Has Diagnostic Value for AECOPD Combined with AKI

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          Abstract

          Background

          In patients with acute exacerbation of chronic obstructive pulmonary disease (AECOPD) complicated by acute kidney injury (AKI) has an acute onset and seriously affects the prognosis of patients. The inflammatory factors are still in doubt in the diagnosis of AECOPD with AKI.

          Material and Methods

          This study is a retrospective study. By collecting the plasma concentrations of inflammatory factors IFN-γ, IL-2, IL-4, IL-10, IL-17, and NGAL in patients with AECOPD group, AECOPD plus AKI group, and control group. The expression level of each factor among the three different groups was analyzed, and the correlation of each factor was analyzed. The diagnostic value of each factor in patients with AECOPD combined with AKI was tested.

          Results

          A total of 245 cases of AECOPD, 69 cases of AECOPD with AKI, and 50 healthy control group were included in this study. IFN-γ and IL-4 were differentially expressed among the three groups (P <0.001). However, there was no difference between the AECOPD group and the AECOPD + AKI group (P = 0.153, and 0.070, respectively). The expression of IL-2, IL-10, IL-17, and NGAL in the three groups were different, and there are statistical differences in pairwise comparisons. (all P values are <0.001). The univariate analysis showed that NGAL and IL-10 with the best correlation (r = 0.696). The ROC curve shows that IL-10 and NGAL have better diagnostic value for AECOPD with AKI.

          Conclusion

          The inflammatory factor IL-10 combined with NGAL has a better diagnostic value for AECOPD with AKI.

          Most cited references24

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          Acute Kidney Injury.

          Acute kidney injury (AKI) is a global public health concern associated with high morbidity, mortality, and healthcare costs. Other than dialysis, no therapeutic interventions reliably improve survival, limit injury, or speed recovery. Despite recognized shortcomings of in vivo animal models, the underlying pathophysiology of AKI and its consequence, chronic kidney disease (CKD), is rich with biological targets. We review recent findings relating to the renal vasculature and cellular stress responses, primarily the intersection of the unfolded protein response, mitochondrial dysfunction, autophagy, and the innate immune response. Maladaptive repair mechanisms that persist following the acute phase promote inflammation and fibrosis in the chronic phase. Here macrophages, growth-arrested tubular epithelial cells, the endothelium, and surrounding pericytes are key players in the progression to chronic disease. Better understanding of these complex interacting pathophysiological mechanisms, their relative importance in humans, and the utility of biomarkers will lead to therapeutic strategies to prevent and treat AKI or impede progression to CKD or end-stage renal disease (ESRD).
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            Renal recovery after acute kidney injury

            Acute kidney injury (AKI) is a frequent complication of critical illness and carries a significant risk of short- and long-term mortality, chronic kidney disease (CKD) and cardiovascular events. The degree of renal recovery from AKI may substantially affect these long-term endpoints. Therefore maximising recovery of renal function should be the goal of any AKI prevention and treatment strategy. Defining renal recovery is far from straightforward due in part to the limitations of the tests available to assess renal function. Here, we discuss common pitfalls in the evaluation of renal recovery and provide suggestions for improved assessment in the future. We review the epidemiology of renal recovery and of the association between AKI and the development of CKD. Finally, we stress the importance of post-discharge follow-up of AKI patients and make suggestions for its incorporation into clinical practice. Summary key points are that risk factors for non-recovery of AKI are age, CKD, comorbidity, higher severity of AKI and acute disease scores. Second, AKI and CKD are mutually related and seem to have a common denominator. Third, despite its limitations full recovery of AKI may best be defined as the absence of AKI criteria, and partial recovery as a fall in AKI stage. Fourth, after an episode of AKI, serial follow-up measurements of serum creatinine and proteinuria are warranted to diagnose renal impairment and prevent further progression. Measures to promote recovery are similar to those preventing renal harm. Specific interventions promoting repair are still experimental.
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              Acute kidney injury 2016: diagnosis and diagnostic workup

              Acute kidney injury (AKI) is common and is associated with serious short- and long-term complications. Early diagnosis and identification of the underlying aetiology are essential to guide management. In this review, we outline the current definition of AKI and the potential pitfalls, and summarise the existing and future tools to investigate AKI in critically ill patients.
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                Author and article information

                Journal
                Int J Chron Obstruct Pulmon Dis
                Int J Chron Obstruct Pulmon Dis
                COPD
                copd
                International Journal of Chronic Obstructive Pulmonary Disease
                Dove
                1176-9106
                1178-2005
                26 March 2020
                2020
                : 15
                : 637-644
                Affiliations
                [1 ]Department of Emergency Medicine, Beijing Chaoyang Hospital Jingxi Branch, Capital Medical University , Beijing 100043, People’s Republic of China
                Author notes
                Correspondence: Yu-Geng Liu Department of Emergency Medicine, Beijing Chaoyang Hospital Jingxi Branch, Capital Medical University , No. 5 Jingyuan Road, Shijingshan District, Beijing100043, People’s Republic of ChinaTel +86-010-51718479 Email yugeng_liu@126.com
                Author information
                http://orcid.org/0000-0002-2536-9256
                Article
                245541
                10.2147/COPD.S245541
                7105373
                32273692
                38937ac6-43eb-4a13-b147-bf05086bb2f8
                © 2020 Wei et al.

                This work is published and licensed by Dove Medical Press Limited. The full terms of this license are available at https://www.dovepress.com/terms.php and incorporate the Creative Commons Attribution – Non Commercial (unported, v3.0) License ( http://creativecommons.org/licenses/by-nc/3.0/). By accessing the work you hereby accept the Terms. Non-commercial uses of the work are permitted without any further permission from Dove Medical Press Limited, provided the work is properly attributed. For permission for commercial use of this work, please see paragraphs 4.2 and 5 of our Terms ( https://www.dovepress.com/terms.php).

                History
                : 10 January 2020
                : 15 March 2020
                Page count
                Figures: 2, Tables: 3, References: 36, Pages: 8
                Categories
                Original Research

                Respiratory medicine
                chronic obstructive pulmonary disease,acute exacerbation,acute kidney injury,inflammatory factors,diagnosis

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