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Ischemia reperfusion kidney

Jonatan Barrera-Chimal, Gabriel R Estrela, Sebastian M Lechner, Sébastien Giraud, Soumaya El Moghrabi, Shiem Kaaki, Peter Kolkhof, Thierry Hauet, Frédéric Jaisser
Acute kidney injury induced by ischemia/reperfusion is an independent risk factor for chronic kidney disease. Macrophage recruitment plays an essential role during the injury and repair phases after an ischemic episode in the kidney. Here we show that the novel non-steroidal mineralocorticoid receptor antagonist finerenone or selective myeloid mineralocorticoid receptor ablation protects against subsequent chronic dysfunction and fibrosis induced by an episode of bilateral kidney ischemia/reperfusion in mice...
March 13, 2018: Kidney International
Ibrahim Batal, Sumit Mohan, Sacha A De Serres, Elena-Rodica Vasilescu, Demetra Tsapepas, Russel J Crew, Shefali S Patel, Geo Serban, Kasi McCune, Syed A Husain, Jae-Hyung Chang, Jan M Herter, Govind Bhagat, Glen S Markowitz, Vivette D D'Agati, Mark A Hardy, Lloyd Ratner, Anil Chandraker
Ischemia-reperfusion injury increases allograft immunogenicity and enhances myeloid dendritic cell maturation and trafficking to recipient's secondary lymphoid tissue. Here, we used postreperfusion biopsies from patients who received kidney allografts from deceased donors between 2006 and 2009 to assess the impact of ischemia-reperfusion damage and myeloid dendritic cell density on subsequent allograft rejection episodes. Histologic changes of severe ischemia-reperfusion damage in postreperfusion biopsies were found to be associated with subsequent rejection episodes and suboptimal allograft survival...
March 13, 2018: Kidney International
Andreas Kling, Katja Jantos, Helmut Mack, Wilfried Hornberger, Gisela Backfisch, Yanbin Lao, Marjoleen Nijsen, Beatrice Rendenbach-Mueller, Achim Moeller
Dysregulation of calpains 1 and 2 has been implicated in a variety of pathological disorders including ischemia/reperfusion injuries, kidney diseases, cataract formation, and neurodegenerative diseases such as Alzheimer's disease (AD). 2-(3-Phenyl-1 H )-pyrazol-1-yl)nicotinamides represent a series of novel and potent calpain inhibitors with high selectivity and in vivo efficacy. However, carbonyl reduction leading to the formation of the inactive hydroxyamide was identified as major metabolic liability in monkey and human, a pathway not reflected by routine absorption, distribution, metabolism, and excretion (ADME) assays...
March 8, 2018: ACS Medicinal Chemistry Letters
Penny S Reynolds, Bernard J Fisher, Jacquelyn McCarter, Christopher Sweeney, Erika J Martin, Paul Middleton, Matthew Ellenberg, Evan Fowler, Donald F Brophy, Alpha A Fowler, Bruce D Spiess, Ramesh Natarajan
BACKGROUND: Coagulopathy and inflammation induced by hemorrhagic shock and traumatic injury are associated with increased mortality and morbidity. Vitamin C (VitC) is an antioxidant with potential protective effects on the pro-inflammatory and pro-coagulant pathways. We hypothesized that high-dose VitC administered as a supplement to fluid resuscitation would attenuate inflammation, coagulation dysfunction, and end-organ tissue damage in a swine model of polytrauma and hemorrhage. METHODS: Male Sinclair swine (n = 24; mean body weight 27 kg) were anesthetized, intubated, mechanically ventilated, and instrumented for physiological monitoring...
March 12, 2018: Journal of Trauma and Acute Care Surgery
Shunta Hori, Mitsuru Tomizawa, Fumisato Maesaka, Takuya Owari, Yosuke Morizawa, Yasushi Nakai, Makito Miyake, Tatsuo Yoneda, Nobumichi Tanaka, Katsunori Yoshida, Kiyohide Fujimoto
BACKGROUND: Page kidney phenomenon is caused by strong renal parenchymal compression and leads to renal hypoperfusion and microvascular ischemia, resulting in renal dysfunction and hypertension. Although the development of Page kidney phenomenon in allograft is rare, most of its cases are induced by allograft biopsy or trauma. We observed a case of Page kidney phenomenon that was induced by unusual causes immediately after kidney transplantation. CASE PRESENTATION: A 66-year-old man, whose wife donated a kidney, underwent ABO-compatible living kidney transplantation...
March 13, 2018: BMC Nephrology
Maryam Maleki, Jalal Hasanshahi, Fatemeh Moslemi
Background: Nitric oxide (NO) as a vasodilator factor has renoprotective effect against renal ischemia. The balance between angiotensin II (Ang II) and NO can affect kidney homeostasis. The aim of this study was to determine NO alteration in response to renin-Ang system vasodilator receptors antagonists (PD123319; Ang II type 2 receptor antagonist and A779; Mas receptor antagonist) in renal ischemia/reperfusion injury (IRI) in rats. Materials and Methods: Sixty-three Wistar male and female rats were used...
2018: Advanced Biomedical Research
Wei Fang, Ziying Wang, Quanxin Li, Xiaojie Wang, Yan Zhang, Yu Sun, Wei Tang, Chunhong Ma, Jinpeng Sun, Ningjun Li, Fan Yi
Background G protein-coupled receptors (GPCRs) participate in a variety of physiologic functions, and several GPCRs have critical physiologic and pathophysiologic roles in the regulation of renal function. We investigated the role of Gpr97, a newly identified member of the adhesion GPCR family, in AKI. Methods AKI was induced by ischemia-reperfusion or cisplatin treatment in Gpr97-deficient mice. We assessed renal injury in these models and in patients with acute tubular necrosis by histologic examination, and we conducted microarray analysis and in vitro assays to determine the molecular mechanisms of Gpr97 function...
March 12, 2018: Journal of the American Society of Nephrology: JASN
Alexandra Kovalčíková, Marianna Gyurászová, Diana Vavrincová-Yaghi, Peter Vavrinec, Ľubomíra Tóthová, Peter Boor, Katarína Šebeková, Peter Celec
Uremic encephalopathy is a severe complication of renal failure. The underlying pathogenesis is unknown although several mechanisms have been suggested. Renal failure causes oxidative stress leading to cardiovascular complications. It has been suggested as the potential mediator of uremic encephalopathy as well, but it is largely unknown whether brain tissue itself undergoes oxidative damage in uremia. The aim of our experiment was to analyze oxidative stress markers in different brain regions in an animal model of acute kidney injury (AKI)...
March 7, 2018: Metabolic Brain Disease
Mitsuhiro Yamamura, Yuji Miyamoto, Masataka Mitsuno, Hiroe Tanaka, Masaaki Ryomoto
Objective : We have previously shown that pretreatment with the free radical scavenger edaravone (Radicut® , Mitsubishi Tanabe Pharma Co., Japan) mitigated skeletal muscle damage due to ischemia reperfusion. In this study, we sought to validate its use in an experimental model of myonephropathic-metabolic syndrome (MNMS). Methods : Either edaravone (3.0 mg/kg; edaravone group; n=4) or saline (saline group; n=6) was intraperitoneally injected into male Lewis rats (508±31 g). Normal kidneys were harvested as control (n=3)...
December 25, 2017: Annals of Vascular Diseases
Jun Kobayashi, Isamu Murata
Crush syndrome is characterized by ischemia/reperfusion injury (IRI). The protective effect of nitrite on experimentally induced IRI has been demonstrated in the heart, kidney, liver, and skeletal muscle. IRI in tissues and systemic organs occurs due to the massive generation of reactive oxygen species and subsequent systemic inflammation. Therefore, ischemic pre and postconditioning are performed in clinical practice. Intravenous administration of nitrite inhibits IRI through nitric oxide-mediated mechanisms...
March 2018: Physiological Reports
Felix C F Schmitt, Eduardo Salgado, Janina Friebe, Thomas Schmoch, Florian Uhle, Thomas Fleming, Johanna Zemva, Lars Kihm, Christian Nusshag, Christian Morath, Martin Zeier, Thomas Bruckner, Arianeb Mehrabi, Peter P Nawroth, Markus A Weigand, Stefan Hofer, Thorsten Brenner
BACKGROUND: A prolonged cold ischemia time (CIT) is suspected to be associated with an increased ischemia and reperfusion injury (IRI) resulting in an increased damage to the graft. METHODS: In total, 91 patients were evaluated for a delayed graft function within 7 days after kidney transplantation (48 deceased, 43 living donors). Blood and urine samples were collected before, immediately after the operation, and 1, 3, 5, 7 and 10 days later. Plasma and/or urine levels of total keratin 18 (total K18), caspase-cleaved keratin 18 (cc K18), the soluble receptor for advanced glycation end-products (sRAGE), tissue inhibitor of metalloproteinase-2 and insulin-like growth factor-binding protein-7 ([TIMP-2]×[IGFBP7]) were measured...
March 5, 2018: Transplant International: Official Journal of the European Society for Organ Transplantation
Bangming Cao, Chi Zhang, Haipeng Wang, Ming Xia, Xiangjun Yang
Background: Whether upper arm remote ischemic postconditioning (RIPostC) exerts protection to kidney in patients with ST-elevation myocardial infarction (STEMI) undergoing primary percutaneous coronary intervention (PPCI) remains unknown. Methods: Sixty-four patients with STEMI were randomized to PPCI + RIPostC (n=29) and PPCI (n=35) groups. RIPostC consisting of 4 cycles of 5 minutes occlusion/reperfusion by cuff inflation/deflation of the upper arm was started within 1 minute after the first balloon dilatation...
2018: Therapeutics and Clinical Risk Management
Anne von Mässenhausen, Wulf Tonnus, Nina Himmerkus, Simon Parmentier, Danish Saleh, Diego Rodriquez, Jiraporn Ousingsawat, Rosalind L Ang, Joel M Weinberg, Ana B Sanz, Alberto Ortiz, Adrian Zierleyn, Jan Ulrich Becker, Blandine Baratte, Nathalie Desban, Stéphane Bach, Ina Maria Schiessl, Shoko Nogusa, Siddharth Balachandran, Hans Joachim Anders, Adrian T Ting, Markus Bleich, Alexei Degterev, Karl Kunzelmann, Stefan R Bornstein, Douglas R Green, Christian Hugo, Andreas Linkermann
Receptor-interacting protein kinases 1 and 3 (RIPK1/3) have best been described for their role in mediating a regulated form of necrosis, referred to as necroptosis. During this process, RIPK3 phosphorylates mixed lineage kinase domain-like (MLKL) to cause plasma membrane rupture. RIPK3-deficient mice have recently been demonstrated to be protected in a series of disease models, but direct evidence for activation of necroptosis in vivo is still limited. Here, we sought to further examine the activation of necroptosis in kidney ischemia-reperfusion injury (IRI) and from TNFα-induced severe inflammatory response syndrome (SIRS), two models of RIPK3-dependent injury...
March 2, 2018: Cell Death & Disease
Tao-Tao Tang, Lin-Li Lv, Ming-Ming Pan, Yi Wen, Bin Wang, Zuo-Lin Li, Min Wu, Feng-Mei Wang, Steve D Crowley, Bi-Cheng Liu
Inflammation is a major contributor to the pathogenesis of ischemic acute kidney injury (AKI), which complicates the post-operative outcomes of large numbers of hospitalized surgical patients. Hydroxychloroquine (HCQ), a well-known anti-malarial drug, is commonly used in clinical practice for its anti-inflammatory actions. However, little is known about its role in renal ischemia/reperfusion (I/R) injury. In the current study, mice were subjected to I/R injury and HCQ was administered for seven days by gavage prior to surgery...
March 2, 2018: Cell Death & Disease
Ying Xie, Daofang Jiang, Jing Xiao, Chensheng Fu, Zhenxing Zhang, Zhibin Ye, Xiaoli Zhang
Ischemic preconditioning (IPC) has a strong renoprotective effect during renal ischemia/reperfusion (I/R) injury that is thought to relate to autophagy. However, the role of autophagy during IPC-afforded renoprotection and the precise mechanisms involved are unknown. In this study, an in vitro hypoxia/reoxygenation (H/R) model was established in which oxygen and glucose deprivation (OGD) was applied to renal cells for 15 h followed by reoxygenation under normal conditions for 30 min, 2 h or 6 h; transient OGD and subsequent reoxygenation were implemented before prolonged H/R injury to achieve hypoxic preconditioning (HPC)...
March 1, 2018: Cell Death & Disease
Marie Ito, Tetsuhiro Tanaka
Sodium-glucose cotransporter 2 (SGLT2), which is specifically expressed on the apical side of proximal tubular cells, is involved in the reabsorption of most of the glucose filtered by the glomeruli, and its inhibitors are gaining publicity as potent antihyperglycemic drugs. In some clinical trials, SGLT2 inhibitors exerted cardiovascular and kidney protective effects, which appeared to be partly independent of the original glucose-lowering effect. SGLT2 inhibitors have both direct and indirect renoprotective effects...
February 28, 2018: Internal Medicine
Jiawei Li, Long Li, Shuo Wang, Chao Zhang, Long Zheng, Yichen Jia, Ming Xu, Tongyu Zhu, Yi Zhang, Ruiming Rong
BACKGROUND: Ischemia-reperfusion injury (IRI) is one of the major causes of postoperative renal allograft dysfunction, which is mainly the result of proinflammatory reactions including inflammatory responses, oxidative stress, and metabolic disorders. Resveratrol (RSV) plays an important role in protecting various organs in IRI because it reduces oxidative stress, lessens the inflammatory response, and exerts anti-apoptotic effects. The aim of this study was to demonstrate the renoprotective effect of RSV in inhibiting inflammatory responses, reducing oxidative stress, and decreasing cell apoptosis in vivo and in vitro...
February 22, 2018: Cellular Physiology and Biochemistry
Bin Xiong, Min Li, Shulin Xiang, Lin Han
PURPOSE: A1 adenosine receptor (AR) activation has been demonstrated to attenuate renal ischemia/reperfusion injury (IRI), but the exact mechanism of this protection remains to be well elucidated. METHODS: Male C57BL/6 mice were used in the present study. Expression of heat shock protein (HSP) 27 and HSF-1 were detected using western blot analysis. An RNA interference with adenovirus vector using short hairpin RNA targeting HSP27 was developed. Together with renal IRI model, indicators of renal function, acute tubular necrosis, inflammation and apoptosis were measured in kidneys after 24-h reperfusion...
February 26, 2018: International Urology and Nephrology
Yi Wen, Yi-Ran Liu, Tao-Tao Tang, Ming-Ming Pan, Sheng-Chun Xu, Kun-Ling Ma, Lin-Li Lv, Hong Liu, Bi-Cheng Liu
Ischemia/reperfusion (I/R) is a critical risk factor for acute kidney injury (AKI). Recent studies provided evidence that tubular epithelial cells (TEC)-associated inflammation aggravates kidney injury and impairs tissue repair after I/R injury. Here we demonstrated that the Nod-like receptor protein 3 (NLRP3) inflammasome is activated by mitochondrial reactive oxygen species (mROS) during I/R injury via direct interactions between the inflammasome and thioredoxin-interacting protein (TXNIP). Firstly, we found that NLRP3 inflammasome activation was induced by I/R injury, peaking at day 3 after reperfusion...
February 22, 2018: International Journal of Biochemistry & Cell Biology
Hester van Willigenburg, Peter L J de Keizer, Ron W F de Bruin
Kidney transplants from aged donors are more vulnerable to ischemic injury, suffer more from delayed graft function and have a lower graft survival compared to kidneys from younger donors. On a cellular level, aging results in an increase in cells that are in a permanent cell cycle arrest, termed senescence, which secrete a range of pro-inflammatory cytokines and growth factors. Consequently, these senescent cells negatively influence the local milieu by causing inflammaging, and by reducing the regenerative capacity of the kidney...
February 19, 2018: Pharmacological Research: the Official Journal of the Italian Pharmacological Society
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