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Advances in Acute Kidney Injury: From Bench to Bedside
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Advances in Acute Kidney Injury: From Bench to Bedside

A special issue of International Journal of Molecular Sciences (ISSN 1422-0067). This special issue belongs to the section "Molecular Pathology, Diagnostics, and Therapeutics".

Deadline for manuscript submissions: closed (31 August 2023) | Viewed by 10222

Special Issue Editors

Prof. Dr. Stuart L. Goldstein

E-Mail Website
Guest Editor
UC Department of Pediatrics, Cincinnati Children's Hospital Medical Center, Cincinnati, OH 45209, USA
Interests: acute kidney injury (AKI); biomarkers; precision medicine; renal recovery; renal angina Index (RAI); risk stratification; targeted treatment for AKI
Dr. Naomi Pode-Shakked

E-Mail Website
Guest Editor
Sackler School of Medicine, Tel Aviv University, Tel Aviv-Yafo, Israel
Interests: acute kidney injury; kidney stem cells; kidney organoids; precision medicine; AKI to CKD; renal repair; regenerative medicine; kidney development

Special Issue Information

Dear Colleagues, 

Acute kidney injury (AKI) is a prevalent condition in hospitalized patients and affects an even larger number of those admitted to intensive care units (ICU). AKI is associated with poor outcomes, as well as increased risk of developing chronic kidney disease (CKD) in the long run. 

The past decade has witnessed major advancements in AKI prediction in ICU patients, utilizing complex prediction scores (i.e., the renal angina index) and unique biomarkers, allowing the detection of at-risk patients for timely interventions. Despite this, treatment options for severe AKI remain limited to supportive care and renal replacement therapy. Novel research models and methodologies for studying the molecular and cellular processes underlying human AKI are therefore urgently needed in order to enable the development of pathomechanism-based, targeted treatment options. Moreover, bridging the bench-to-bedside interface through translating basic findings for the improvement of clinical care and severe AKI patient outcomes is a crucial next step.

We are pleased to invite you to contribute to this Special Issue, where we aim to showcase the latest translational insights into AKI pathomechanisms, molecular pathways, diagnosis, predictive models and interventions.

This Special Issue aims to provide the readership with the latest discoveries in the field, including (but not limited to) the following:

  • Pathomechanisms contributing to the transition of acute kidney injury (AKI) to chronic kidney disease (CKD).
  • Cutting-edge models for the study of specific types of AKI.
  • Novel biomarkers for the early detection of nephrotoxicity.
  • Cellular and molecular mechanisms involved in kidney injury, repair and fibrosis following AKI.
  • Novel methodologies for optimization of tissue acquisition, processing, examination and data interpretation to improve our understanding of the cellular and molecular heterogeneity of human AKI.
  • Molecular-based subtyping of human AKI and mechanism-based treatment approaches.
  • New approaches for the prediction of severe AKI in critically ill patients, oncologic patients receiving chemotherapy, etc.
  • Development of targeted treatments for AKI.

For submission to this Special Issue, original research articles and reviews are welcome. Case reports will not be considered for publication.

We look forward to receiving your valued contributions.

Prof. Dr. Stuart L. Goldstein
Dr. Naomi Pode-Shakked
Guest Editors

Manuscript Submission Information

Manuscripts should be submitted online at www.mdpi.com by registering and logging in to this website. Once you are registered, click here to go to the submission form. Manuscripts can be submitted until the deadline. All submissions that pass pre-check are peer-reviewed. Accepted papers will be published continuously in the journal (as soon as accepted) and will be listed together on the special issue website. Research articles, review articles as well as short communications are invited. For planned papers, a title and short abstract (about 100 words) can be sent to the Editorial Office for announcement on this website.

Submitted manuscripts should not have been published previously, nor be under consideration for publication elsewhere (except conference proceedings papers). All manuscripts are thoroughly refereed through a single-blind peer-review process. A guide for authors and other relevant information for submission of manuscripts is available on the Instructions for Authors page. International Journal of Molecular Sciences is an international peer-reviewed open access semimonthly journal published by MDPI.

Please visit the Instructions for Authors page before submitting a manuscript. There is an Article Processing Charge (APC) for publication in this open access journal. For details about the APC please see here. Submitted papers should be well formatted and use good English. Authors may use MDPI's English editing service prior to publication or during author revisions.

Keywords

  • acute kidney injury (AKI)
  • biomarkers
  • precision medicine
  • renal recovery
  • renal angina Index (RAI)
  • risk stratification
  • targeted treatment for AKI

Published Papers (5 papers)

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26 pages, 11134 KiB  
Article
GADD45A and GADD45B as Novel Biomarkers Associated with Chromatin Regulators in Renal Ischemia-Reperfusion Injury
by Ming Xie, Ruiyan Xie, Pengcheng Huang, Desmond Y. H. Yap and Peng Wu
Int. J. Mol. Sci. 2023, 24(14), 11304; https://doi.org/10.3390/ijms241411304 - 11 Jul 2023
Cited by 2 | Viewed by 1763
Abstract
Chromatin regulators (CRs) are essential upstream regulatory factors of epigenetic modification. The role of CRs in the pathogenesis of renal ischemia-reperfusion injury (IRI) remains unclear. We analyzed a bioinformatic analysis on the differentially expressed chromatin regulator genes in renal IRI patients using data [...] Read more.
Chromatin regulators (CRs) are essential upstream regulatory factors of epigenetic modification. The role of CRs in the pathogenesis of renal ischemia-reperfusion injury (IRI) remains unclear. We analyzed a bioinformatic analysis on the differentially expressed chromatin regulator genes in renal IRI patients using data from public domains. The hub CRs identified were used to develop a risk prediction model for renal IRI, and their expressions were also validated using Western blot, qRT-PCR, and immunohistochemistry in a murine renal IRI model. We also examined the relationships between hub CRs and infiltrating immune cells in renal IRI and used network analysis to explore drugs that target hub CRs and their relevant downstream microRNAs. The results of machine learning methods showed that five genes (DUSP1, GADD45A, GADD45B, GADD45G, HSPA1A) were upregulated in renal IRI, with key roles in the cell cycle, p38 MAPK signaling pathway, p53 signaling pathway, FoxO signaling pathway, and NF-κB signaling pathway. Two genes from the network, GADD45A and GADD45B (growth arrest and DNA damage-inducible protein 45 alpha and beta), were chosen for the renal IRI risk prediction model. They all showed good performance in the testing and validation cohorts. Mice with renal IRI showed significantly upregulated GADD45A and GADD45B expression within kidneys compared to sham-operated mice. GADD45A and GADD45B showed correlations with plasmacytoid dendritic cells (pDCs) in infiltrating immune cell analysis and enrichment in the MAPK pathway based on the weighted gene co-expression network analysis (WGCNA) method. Candidate drugs that target GADD45A and GADD45B include beta-escin, sertraline, primaquine, pimozide, and azacyclonol. The dysregulation of GADD45A and GADD45B is related to renal IRI and the infiltration of pDCs, and drugs that target GADD45A and GADD45B may have therapeutic potential for renal IRI. Full article
(This article belongs to the Special Issue Advances in Acute Kidney Injury: From Bench to Bedside)
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21 pages, 1095 KiB  
Review
Pathway from Acute Kidney Injury to Chronic Kidney Disease: Molecules Involved in Renal Fibrosis
by Andrei Niculae, Mihai-Emil Gherghina, Ileana Peride, Mirela Tiglis, Ana-Maria Nechita and Ionel Alexandru Checherita
Int. J. Mol. Sci. 2023, 24(18), 14019; https://doi.org/10.3390/ijms241814019 - 13 Sep 2023
Cited by 2 | Viewed by 1735
Abstract
Acute kidney injury (AKI) is one of the main conditions responsible for chronic kidney disease (CKD), including end-stage renal disease (ESRD) as a long-term complication. Besides short-term complications, such as electrolyte and acid-base disorders, fluid overload, bleeding complications or immune dysfunctions, AKI can [...] Read more.
Acute kidney injury (AKI) is one of the main conditions responsible for chronic kidney disease (CKD), including end-stage renal disease (ESRD) as a long-term complication. Besides short-term complications, such as electrolyte and acid-base disorders, fluid overload, bleeding complications or immune dysfunctions, AKI can develop chronic injuries and subsequent CKD through renal fibrosis pathways. Kidney fibrosis is a pathological process defined by excessive extracellular matrix (ECM) deposition, evidenced in chronic kidney injuries with maladaptive architecture restoration. So far, cited maladaptive kidney processes responsible for AKI to CKD transition were epithelial, endothelial, pericyte, macrophage and fibroblast transition to myofibroblasts. These are responsible for smooth muscle actin (SMA) synthesis and abnormal renal architecture. Recently, AKI progress to CKD or ESRD gained a lot of interest, with impressive progression in discovering the mechanisms involved in renal fibrosis, including cellular and molecular pathways. Risk factors mentioned in AKI progression to CKD are frequency and severity of kidney injury, chronic diseases such as uncontrolled hypertension, diabetes mellitus, obesity and unmodifiable risk factors (i.e., genetics, older age or gender). To provide a better understanding of AKI transition to CKD, we have selected relevant and updated information regarding the risk factors responsible for AKIs unfavorable long-term evolution and mechanisms incriminated in the progression to a chronic state, along with possible therapeutic approaches in preventing or delaying CKD from AKI. Full article
(This article belongs to the Special Issue Advances in Acute Kidney Injury: From Bench to Bedside)
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20 pages, 2610 KiB  
Article
Calorie Restriction Provides Kidney Ischemic Tolerance in Senescence-Accelerated OXYS Rats
by Nadezda V. Andrianova, Ljubava D. Zorova, Irina B. Pevzner, Nataliya G. Kolosova, Egor Y. Plotnikov and Dmitry B. Zorov
Int. J. Mol. Sci. 2022, 23(23), 15224; https://doi.org/10.3390/ijms232315224 - 03 Dec 2022
Cited by 1 | Viewed by 1714
Abstract
Kidney diseases belong to a group of pathologies, which are most common among elderly people. With age, even outwardly healthy organisms start to exhibit some age-related changes in the renal tissue, which reduce the filtration function of kidneys and increase the susceptibility to [...] Read more.
Kidney diseases belong to a group of pathologies, which are most common among elderly people. With age, even outwardly healthy organisms start to exhibit some age-related changes in the renal tissue, which reduce the filtration function of kidneys and increase the susceptibility to injury. The therapy of acute kidney injury (AKI) is aggravated by the absence of targeted pharmacotherapies thus yielding high mortality of patients with AKI. In this study, we analyzed the protective effects of calorie restriction (CR) against ischemic AKI in senescence-accelerated OXYS rats. We observed that CR afforded OXYS rats with significant nephroprotection. To uncover molecular mechanisms of CR beneficial effects, we assessed the levels of anti- and proapoptotic proteins of the Bcl-2 family, COX IV, GAPDH, and mitochondrial deacetylase SIRT-3, as well as alterations in total protein acetylation and carbonylation, mitochondrial dynamics (OPA1, Fis1, Drp1) and kidney regeneration pathways (PCNA, GDF11). The activation of autophagy and mitophagy was analyzed by LC3 II/LC3 I ratio, beclin-1, PINK-1, and total mitochondrial protein ubiquitination. Among all considered protective pathways, the improvement of mitochondrial functioning may be suggested as one of the possible mechanisms for beneficial effects of CR. Full article
(This article belongs to the Special Issue Advances in Acute Kidney Injury: From Bench to Bedside)
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16 pages, 17767 KiB  
Article
Identification of Pre-Renal and Intrinsic Acute Kidney Injury by Anamnestic and Biochemical Criteria: Distinct Association with Urinary Injury Biomarkers
by Sandra M. Sancho-Martínez, Alfredo G. Casanova, Annette G. Düwel, Karen Rivero-García, Tamara García-Garrido, Ana I. Morales, Carlos Martínez-Salgado, Francisco J. López-Hernández and Pilar Fraile
Int. J. Mol. Sci. 2023, 24(3), 1826; https://doi.org/10.3390/ijms24031826 - 17 Jan 2023
Cited by 1 | Viewed by 2139
Abstract
Acute kidney injury (AKI) is a syndrome of sudden renal excretory dysfunction with severe health consequences. AKI etiology influences prognosis, with pre-renal showing a more favorable evolution than intrinsic AKI. Because the international diagnostic criteria (i.e., based on plasma creatinine) provide no etiological [...] Read more.
Acute kidney injury (AKI) is a syndrome of sudden renal excretory dysfunction with severe health consequences. AKI etiology influences prognosis, with pre-renal showing a more favorable evolution than intrinsic AKI. Because the international diagnostic criteria (i.e., based on plasma creatinine) provide no etiological distinction, anamnestic and additional biochemical criteria complement AKI diagnosis. Traditional, etiology-defining biochemical parameters, including the fractional excretion of sodium, the urinary-to-plasma creatinine ratio and the renal failure index are individually limited by confounding factors such as diuretics. To minimize distortion, we generated a composite biochemical criterion based on the congruency of at least two of the three biochemical ratios. Patients showing at least two ratios indicative of intrinsic AKI were classified within this category, and those with at least two pre-renal ratios were considered as pre-renal AKI patients. In this study, we demonstrate that the identification of intrinsic AKI by a collection of urinary injury biomarkers reflective of tubular damage, including NGAL and KIM-1, more closely and robustly coincide with the biochemical than with the anamnestic classification. Because there is no gold standard method for the etiological classification of AKI, the mutual reinforcement provided by the biochemical criterion and urinary biomarkers supports an etiological diagnosis based on objective diagnostic parameters. Full article
(This article belongs to the Special Issue Advances in Acute Kidney Injury: From Bench to Bedside)
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13 pages, 1729 KiB  
Article
The Novel Compound SUL-138 Counteracts Endothelial Cell and Kidney Dysfunction in Sepsis by Preserving Mitochondrial Function
by Bastiaan S. Star, Elisabeth C. van der Slikke, Azuwerus van Buiten, Robert H. Henning and Hjalmar R. Bouma
Int. J. Mol. Sci. 2023, 24(7), 6330; https://doi.org/10.3390/ijms24076330 - 28 Mar 2023
Cited by 2 | Viewed by 2171
Abstract
Sepsis is defined as a dysregulated host response leading to organ dysfunction, which may ultimately result in the patient’s death. Mitochondrial dysfunction plays a key role in developing organ dysfunction in sepsis. In this study, we explored the efficacy of the novel mitochondrial [...] Read more.
Sepsis is defined as a dysregulated host response leading to organ dysfunction, which may ultimately result in the patient’s death. Mitochondrial dysfunction plays a key role in developing organ dysfunction in sepsis. In this study, we explored the efficacy of the novel mitochondrial protective compound, SUL-138, in sepsis models in HUVECs and mice. In LPS-challenged HUVECs, SUL-138 preserved mitochondrial membrane potential and oxygen consumption and limited mitochondrial oxidative stress, resulting in increased survival at 48 h. Further, SUL-138 dampened the LPS-induced expression of IL-1β, but not of NLRP3, and IL-18 in HUVECs. Sepsis in mice induced by cecal ligation and puncture (CLP) led to a lower mitochondrial membrane potential and increased levels of mitochondrial oxidative stress in the kidney, which SUL-138 limited. In addition, SUL-138 mitigated the CLP-induced increase in kidney dysfunction markers NGAL and urea. It dampened the rise in kidney expression of IL-6, IL-1β, and ICAM-1, but not TNF-α and E-selectin. Yet, SUL-138 limited the increase in plasma levels of IL-6 and TNF-α of CLP mice. These results demonstrate that SUL-138 supports mitochondrial function, resulting in a limitation of systemic inflammation and preservation of kidney function. Full article
(This article belongs to the Special Issue Advances in Acute Kidney Injury: From Bench to Bedside)
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