7
views
0
recommends
+1 Recommend
0 collections
    0
    shares
      • Record: found
      • Abstract: found
      • Article: found
      Is Open Access

      Association between inflammatory-response gene polymorphisms and risk of acute kidney injury in children

      research-article

      Read this article at

      Bookmark
          There is no author summary for this article yet. Authors can add summaries to their articles on ScienceOpen to make them more accessible to a non-specialist audience.

          Abstract

          In the present study, we investigated the association of 12 polymorphisms in six inflammatory-response genes ( TNF, IL6, IL10, IL18, NFKB1 and NFKBIA) with risk of acute kidney injury (AKI) in children. The polymorphisms were genotyped in 1138 children with AKI and 1382 non-AKI controls. Logistic regression analysis was performed to calculate the odds ratio for estimating the risk association. After accounting for Bonferroni correction and adjustment for potential confounders, significant association was observed for NFKB1 rs28362491, NFKBIA rs2233406 and NFKBIA rs696 polymorphisms ( P < 0.004). All three polymorphisms were associated with a reduced risk of AKI. For rs28362491 polymorphism, the OR for ID vs. II comparison was 0.75 (95% CI = 0.58–0.83) while that for DD vs. II was 0.44 (95% CI = 0.30–0.67). For rs2233406 polymorphism, the CT vs. CC comparison showed an OR of 0.90 (95% CI = 0.39–0.99), while the TT vs. CC comparison showed an OR of 0.43 (95% CI = 0.33–0.80). For rs696 polymorphism, the OR for AG vs. AA comparison was 0.71 (95% CI = 0.43–0.89), while the GG vs. AA comparison showed an OR of 0.39 (95% CI = 0.21–0.71). In conclusion, NFKB1 rs28362491, NFKBIA rs2233406 and NFKBIA rs696 polymorphisms may serve as biomarkers for predicting risk of AKI in children.

          Related collections

          Most cited references25

          • Record: found
          • Abstract: found
          • Article: found
          Is Open Access

          Mediators of Inflammation in Acute Kidney Injury

          Acute kidney injury (AKI) remains to be an independent risk factor for mortality and morbidity. Inflammation is now believed to play a major role in the pathopathophysiology of AKI. It is hypothesized that in ischemia, sepsis and nephrotoxic models that the initial insult results in morphological and/or functional changes in vascular endothelial cells and/or in tubular epithelium. Then, leukocytes including neutrophils, macrophages, natural killer cells, and lymphocytes infiltrate into the injured kidneys. The injury induces the generation of inflammatory mediators like cytokines and chemokines by tubular and endothelial cells which contribute to the recruiting of leukocytes into the kidneys. Thus, inflammation has an important role in the initiation and extension phases of AKI. This review will focus on the mediators of inflammation contributing to the pathogenesis of AKI.
            Bookmark
            • Record: found
            • Abstract: found
            • Article: found
            Is Open Access

            Interleukin-6 Signaling Pathway and Its Role in Kidney Disease: An Update

            Interleukin-6 (IL-6) is a pleiotropic cytokine that not only regulates the immune and inflammatory response but also affects hematopoiesis, metabolism, and organ development. IL-6 can simultaneously elicit distinct or even contradictory physiopathological processes, which is likely discriminated by the cascades of signaling pathway, termed classic and trans-signaling. Besides playing several important physiological roles, dysregulated IL-6 has been demonstrated to underlie a number of autoimmune and inflammatory diseases, metabolic abnormalities, and malignancies. This review provides an overview of basic concept of IL-6 signaling pathway as well as the interplay between IL-6 and renal-resident cells, including podocytes, mesangial cells, endothelial cells, and tubular epithelial cells. Additionally, we summarize the roles of IL-6 in several renal diseases, such as IgA nephropathy, lupus nephritis, diabetic nephropathy, acute kidney injury, and chronic kidney disease.
              Bookmark
              • Record: found
              • Abstract: found
              • Article: found

              Inflammation in Acute Kidney Injury

              Ischemia-reperfusion injury (IRI) is one of the major causes of acute kidney injury (AKI) and evidence supporting the involvement of both innate and adaptive immunity in renal IRI has accumulated in recent years. In addition to leukocytes, kidney endothelial cells promote inflammation after IRI by increasing adhesion molecule expression and vascular permeability. Kidney tubular epithelial cells increase complement binding and upregulate toll-like receptors, both of which lead to cytokine/chemokine production in IRI. Activation of kidney resident dendritic cells, interferon-γ-producing neutrophils, infiltrating macrophages, CD4+ T cells, B cells and invariant natural killer T cells are all implicated in the pathogenesis of AKI. The complex interplay between innate and adaptive immunity in renal IRI is still not completely understood, but major advances have been made. This review summarizes these recent advances to further our understanding of the immune mechanisms of acute kidney injury.
                Bookmark

                Author and article information

                Journal
                Biosci Rep
                Biosci. Rep
                ppbioscirep
                BSR
                Bioscience Reports
                Portland Press Ltd.
                0144-8463
                1573-4935
                14 November 2018
                14 December 2018
                21 December 2018
                : 38
                : 6
                : BSR20180537
                Affiliations
                [1 ]Department of Pediatrics, The First People’s Hospital of Bijie, Bijie 551700, Guizhou Province, China
                [2 ]Department of Radiology, The First People’s Hospital of Bijie, Bijie 551700, Guizhou Province, China
                [3 ]Department of Clinical Laboratory, The First People’s Hospital of Bijie, Bijie 551700, Guizhou Province, China
                Author notes
                Correspondence: Xinqian Zhao ( zuqkg40@ 123456163.com )
                Author information
                http://orcid.org/0000-0001-7330-3430
                Article
                10.1042/BSR20180537
                6294618
                30429237
                bb728928-a2d0-416d-a523-da2d47af945b
                © 2018 The Author(s).

                This is an open access article published by Portland Press Limited on behalf of the Biochemical Society and distributed under the Creative Commons Attribution License 4.0 (CC BY).

                History
                : 07 April 2018
                : 31 October 2018
                : 06 November 2018
                Page count
                Pages: 10
                Categories
                Research Articles
                Research Article
                42
                46

                Life sciences
                acute kidney injury (aki),biomarkers,inflammation,pediatric,polymorphisms
                Life sciences
                acute kidney injury (aki), biomarkers, inflammation, pediatric, polymorphisms

                Comments

                Comment on this article