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Kidney Transplantation, Ischemia Reperfusion, Organ Quality and Acute Kidney Injury

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A special issue of International Journal of Molecular Sciences (ISSN 1422-0067). This special issue belongs to the section "Molecular Role of Xenobiotics".

Deadline for manuscript submissions: closed (31 January 2022) | Viewed by 14645

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Special Issue Editor

Dr. Raphaël Thuillier

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Guest Editor

1. Faculté de Médecine et de Pharmacie, Université de Poitiers, F-86000 Poitiers, France
2. Inserm U1082, F-86000 Poitiers, France
3. CHU Poitiers, Service de Biochimie, F-86021 Poitiers, France
Interests: ischemia reperfusion; organ preservation; organ quality; acute and chronic kidney injury
Special Issues, Collections and Topics in MDPI journals

Special Issue Information

Dear Colleagues,

Kidney transplantation is the best therapy to treat chronic renal failure. However, it has become a victim of its success, as the number of kidney transplantations is far behind the number of patients on the waiting list, leading to drastic changes in donor demography, with a large proportion of organs now issued from marginal donors, much more sensible to the stresses of transplantation, chief among which ischemia-reperfusion injury (IRI). This syndrome is a key therapeutic target to improve organ quality and decrease transplantation-related acute kidney injury (AKI), a serious complication which without an efficient curative approach will shift toward chronic kidney injury.

The healthcare community is thus in need for novel approaches to better manage the transplantation process, from innovative organ preservation approaches, to better donor management, increased understanding of graft quality, and prognostic tools to anticipate complication.

I am pleased to invite all of you to participate to this Special Issue, “Kidney Transplantation, Ischemia Reperfusion, Organ Quality, and Acute Kidney Injury”, by presenting your most recent research or ideas on these issues. Experimental papers, up-to-date review articles, and commentaries are all welcome.

Dr. Raphael Thuillier
Guest Editor

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

Ischemia reperfusion
Organ preservation
Organ quality
Acute kidney injury
Chronic kidney injury

Published Papers (6 papers)

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Research

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21 pages, 53798 KiB

Open AccessArticle

Study of the Role of the Tyrosine Kinase Receptor MerTK in the Development of Kidney Ischemia-Reperfusion Injury in RCS Rats

by Thomas Pelé, Sebastien Giraud, Sandrine Joffrion, Virginie Ameteau, Adriana Delwail, Jean-Michel Goujon, Laurent Macchi, Thierry Hauet, Fatima Dkhissi and Omar Benzakour

Int. J. Mol. Sci. 2021, 22(22), 12103; https://doi.org/10.3390/ijms222212103 - 09 Nov 2021

Cited by 2 | Viewed by 2083

Abstract

Renal ischaemia reperfusion (I/R) triggers a cascade of events including oxidative stress, apoptotic body and microparticle (MP) formation as well as an acute inflammatory process that may contribute to organ failure. Macrophages are recruited to phagocytose cell debris and MPs. The tyrosine kinase receptor MerTK is a major player in the phagocytosis process. Experimental models of renal I/R events are of major importance for identifying I/R key players and for elaborating novel therapeutical approaches. A major aim of our study was to investigate possible involvement of MerTK in renal I/R. We performed our study on both natural mutant rats for MerTK (referred to as RCS) and on wild type rats referred to as WT. I/R was established by of bilateral clamping of the renal pedicles for 30′ followed by three days of reperfusion. Plasma samples were analysed for creatinine, aspartate aminotransferase (ASAT), lactate dehydrogenase (LDH), kidney injury molecule -1 (KIM-1), and neutrophil gelatinase-associated lipocalin (NGAL) levels and for MPs. Kidney tissue damage and CD68-positive cell requirement were analysed by histochemistry. monocyte chemoattractant protein-1 (MCP-1), myeloperoxidase (MPO), inducible nitric oxide synthase (iNOS), and histone 3A (H3A) levels in kidney tissue lysates were analysed by western blotting. The phagocytic activity of blood-isolated monocytes collected from RCS or WT towards annexin-V positive bodies derived from cultured renal cell was assessed by fluorescence-activated single cell sorting (FACS) and confocal microscopy analyses. The renal I/R model for RCS rat described for the first time here paves the way for further investigations of MerTK-dependent events in renal tissue injury and repair mechanisms. Full article

(This article belongs to the Special Issue Kidney Transplantation, Ischemia Reperfusion, Organ Quality and Acute Kidney Injury)

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17 pages, 73948 KiB

Open AccessArticle

Anaesthesia-Induced Transcriptomic Changes in the Context of Renal Ischemia Uncovered by the Use of a Novel Clamping Device

by Charles Verney, David Legouis, Sandrine Placier, Tiffany Migeon, Philippe Bonnin, David Buob, Juliette Hadchouel and Pierre Galichon

Int. J. Mol. Sci. 2021, 22(18), 9840; https://doi.org/10.3390/ijms22189840 - 11 Sep 2021

Cited by 3 | Viewed by 1884

Abstract

Ischemia is a common cause of acute kidney injury worldwide, frequently occurring in patients undergoing cardiac surgery or admitted to the intensive care unit (ICU). Thus, ischemia-reperfusion injury (IRI) remains one of the main experimental models for the study of kidney diseases. However, the classical technique, based on non-traumatic surgical clamps, suffers from several limitations. It does not allow the induction of multiple episodes of acute kidney injury (AKI) in the same animal, which would be relevant from a human perspective. It also requires a deep and long sedation, raising the question of potential anaesthesia-related biases. We designed a vascular occluding device that can be activated remotely in conscious mice. We first assessed the intensity and the reproducibility of the acute kidney injury induced by this new device. We finally investigated the role played by the anaesthesia in the IRI models at the histological, functional and transcriptomic levels. We showed that this technique allows the rapid induction of renal ischemia in a repeatable and reproducible manner, breaking several classical limitations. In addition, we used its unique specificities to highlight the renal protective effect conferred by the anaesthesia, related to the mitigation of the IRI transcriptomic program. Full article

(This article belongs to the Special Issue Kidney Transplantation, Ischemia Reperfusion, Organ Quality and Acute Kidney Injury)

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13 pages, 3190 KiB

Open AccessArticle

A Sodium Oxalate-Rich Diet Induces Chronic Kidney Disease and Cardiac Dysfunction in Rats

by Thayane Crestani, Renato O. Crajoinas, Leonardo Jensen, Leno L. Dima, Perrine Burdeyron, Thierry Hauet, Sebastien Giraud and Clara Steichen

Int. J. Mol. Sci. 2021, 22(17), 9244; https://doi.org/10.3390/ijms22179244 - 26 Aug 2021

Cited by 2 | Viewed by 2170

Abstract

Chronic kidney disease (CKD) is a worldwide public health issue affecting 14% of the general population. However, research focusing on CKD mechanisms/treatment is limited because of a lack of animal models recapitulating the disease physiopathology, including its complications. We analyzed the effects of a three-week diet rich in sodium oxalate (OXA diet) on rats and showed that, compared to controls, rats developed a stable CKD with a 60% reduction in glomerular filtration rate, elevated blood urea levels and proteinuria. Histological analyses revealed massive cortical disorganization, tubular atrophy and fibrosis. Males and females were sensitive to the OXA diet, but decreasing the diet period to one week led to GFR significance but not stable diminution. Rats treated with the OXA diet also displayed classical CKD complications such as elevated blood pressure and reduced hematocrit. Functional cardiac analyses revealed that the OXA diet triggered significant cardiac dysfunction. Altogether, our results showed the feasibility of using a convenient and non-invasive strategy to induce CKD and its classical systemic complications in rats. This model, which avoids kidney mass loss or acute toxicity, has strong potential for research into CKD mechanisms and novel therapies, which could protect and postpone the use of dialysis or transplantation. Full article

(This article belongs to the Special Issue Kidney Transplantation, Ischemia Reperfusion, Organ Quality and Acute Kidney Injury)

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16 pages, 16371 KiB

Open AccessArticle

MiR-126-3p Is Dynamically Regulated in Endothelial-to-Mesenchymal Transition during Fibrosis

by Nina P. Jordan, Samuel J. Tingle, Victoria G. Shuttleworth, Katie Cooke, Rachael E. Redgrave, Esha Singh, Emily K. Glover, Hafiza B. Ahmad Tajuddin, John A. Kirby, Helen M. Arthur, Chris Ward, Neil S. Sheerin and Simi Ali

Int. J. Mol. Sci. 2021, 22(16), 8629; https://doi.org/10.3390/ijms22168629 - 11 Aug 2021

Cited by 14 | Viewed by 2877

Abstract

In fibrotic diseases, myofibroblasts derive from a range of cell types including endothelial-to-mesenchymal transition (EndMT). Increasing evidence suggests that miRNAs are key regulators in biological processes but their profile is relatively understudied in EndMT. In human umbilical vein endothelial cells (HUVEC), EndMT was induced by treatment with TGFβ2 and IL1β. A significant decrease in endothelial markers such as VE-cadherin, CD31 and an increase in mesenchymal markers such as fibronectin were observed. In parallel, miRNA profiling showed that miR-126-3p was down-regulated in HUVECs undergoing EndMT and over-expression of miR-126-3p prevented EndMT, maintaining CD31 and repressing fibronectin expression. EndMT was investigated using lineage tracing with transgenic Cdh5-Cre-ERT2; Rosa26R-stop-YFP mice in two established models of fibrosis: cardiac ischaemic injury and kidney ureteric occlusion. In both cardiac and kidney fibrosis, lineage tracing showed a significant subpopulation of endothelial-derived cells expressed mesenchymal markers, indicating they had undergone EndMT. In addition, miR-126-3p was restricted to endothelial cells and down-regulated in murine fibrotic kidney and heart tissue. These findings were confirmed in patient kidney biopsies. MiR-126-3p expression is restricted to endothelial cells and is down-regulated during EndMT. Over-expression of miR-126-3p reduces EndMT, therefore, it could be considered for miRNA-based therapeutics in fibrotic organs. Full article

(This article belongs to the Special Issue Kidney Transplantation, Ischemia Reperfusion, Organ Quality and Acute Kidney Injury)

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26 pages, 3270 KiB

Open AccessArticle

High Throughput Proteomic Exploration of Hypothermic Preservation Reveals Active Processes within the Cell Associated with Cold Ischemia Kinetic

by Ophélie Pasini-Chabot, Julia Vincent, Sylvain Le Pape, Maryne Lepoittevin, Wassim Kaaki, Jean-Baptiste Woillard, Sebastien Giraud, Nicolas Bourmeyster, Thierry Hauet and Raphael Thuillier

Int. J. Mol. Sci. 2021, 22(5), 2384; https://doi.org/10.3390/ijms22052384 - 27 Feb 2021

Cited by 2 | Viewed by 1708

Abstract

The demand for organs to be transplanted increases pressure on procurement centers, to the detriment of organ quality, increasing complications. New preservation protocols are urgently needed, requiring an in-depth understanding of ischemia-reperfusion mechanisms. We performed a proteomic analysis using LC-MS/MS-TOF data analyzed through R software and Cytoscape’s ClueGO application, comparing the proteome of kidney endothelial cells, key cell type, subjected to 3, 6, 12, 19, and 24 h of cold ischemia and 6 h reperfusion. Critical pathways such as energy metabolism, cytoskeleton structure/transport system, and gene transcription/translation were modulated. Important time windows were revealed: a—during the first 3 h, central proteins were upregulated within these pathways; b—the majority of these upregulations were maintained until 12 h cold ischemia time (CIT); c—after that time, the overall decrease in protein expression was observed; d—at reperfusion, proteins expressed in response to cold ischemia were all downregulated. This shows that cold ischemia is not a simple slowing down of metabolism, as deep changes take place within the proteome on major pathways. Time-sensitive expression of key protein reveals possible quality biomarkers as well as potential targets for new strategies to maintain or optimize organ quality. Full article

(This article belongs to the Special Issue Kidney Transplantation, Ischemia Reperfusion, Organ Quality and Acute Kidney Injury)

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Review

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23 pages, 14513 KiB

Open AccessReview

Molecular Aspects of Volatile Anesthetic-Induced Organ Protection and Its Potential in Kidney Transplantation

by Gertrude J. Nieuwenhuijs-Moeke, Dirk J. Bosch and Henri G.D. Leuvenink

Int. J. Mol. Sci. 2021, 22(5), 2727; https://doi.org/10.3390/ijms22052727 - 08 Mar 2021

Cited by 7 | Viewed by 3108

Abstract

Ischemia reperfusion injury (IRI) is inevitable in kidney transplantation and negatively impacts graft and patient outcome. Reperfusion takes place in the recipient and most of the injury following ischemia and reperfusion occurs during this reperfusion phase; therefore, the intra-operative period seems an attractive window of opportunity to modulate IRI and improve short- and potentially long-term graft outcome. Commonly used volatile anesthetics such as sevoflurane and isoflurane have been shown to interfere with many of the pathophysiological processes involved in the injurious cascade of IRI. Therefore, volatile anesthetic (VA) agents might be the preferred anesthetics used during the transplantation procedure. This review highlights the molecular and cellular protective points of engagement of VA shown in in vitro studies and in vivo animal experiments, and the potential translation of these results to the clinical setting of kidney transplantation. Full article

(This article belongs to the Special Issue Kidney Transplantation, Ischemia Reperfusion, Organ Quality and Acute Kidney Injury)

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