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AKI Repair

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16 papers 0 to 25 followers
By Isabel Acosta-Ochoa Nephrology senior staff. Valladolid. Spain
Xiangjun Zhou, Wei Zhang, Qisheng Yao, Hao Zhang, Guie Dong, Ming Zhang, Yutao Liu, Jian-Kang Chen, Zheng Dong
Kidney repair following injury involves the reconstitution of a structurally and functionally intact tubular epithelium. Growth factors and their receptors, such as EGFR, are important in the repair of renal tubules. Exosomes are cell-produced small (~100nm in diameter) vesicles that contain and transfer proteins, lipids, RNAs and DNAs between cells. In this study, we examined the relationship between exosome production and EGFR activation, and the potential role of exosome in wound healing. EGFR activation occurred shortly after scratch wounding in renal tubular cells...
March 29, 2017: American Journal of Physiology. Renal Physiology
Wesley Hayes
Acute kidney injury (AKI) is common in children admitted to hospital. Whilst some recover normal kidney function following an acute kidney insult, a significant proportion experience long-term sequelae. The aim of this review is to summarize current understanding of the processes that can lead to sequelae following AKI. Kidney injury, repair, recovery and progression are described. Risk factors for progression are outlined, and potential strategies to stratify the risk of progression in children with AKI are discussed...
February 15, 2017: Pediatric Nephrology: Journal of the International Pediatric Nephrology Association
Sarah C Huen, Lloyd G Cantley
Acute kidney injury (AKI) is a growing global health concern, yet no treatment is currently available to prevent it or to promote kidney repair after injury. Animal models demonstrate that the macrophage is a major contributor to the inflammatory response to AKI. Emerging data from human biopsies also corroborate the presence of macrophages in AKI and their persistence in progressive chronic kidney disease. Macrophages are phagocytic innate immune cells that are important mediators of tissue homeostasis and host defense...
February 10, 2017: Annual Review of Physiology
Jeffrey D Pressly, Frank Park
Ischemia-reperfusion injury (IRI) is a common cause of acute kidney injury leading to an induction of oxidative stress, cellular dysfunction, and loss of renal function. DNA damage, including oxidative base modifications and physical DNA strand breaks, is a consequence of renal IRI. Like many other organs in the body, a redundant and highly conserved set of endogenous repair pathways have evolved to selectively recognize the various types of cellular DNA damage and combat its negative effects on cell viability...
April 1, 2017: American Journal of Physiology. Renal Physiology
Monica Chang-Panesso, Benjamin D Humphreys
Terminally differentiated cells can be reprogrammed to pluripotency or directly to another differentiated cell type in vitro, a capacity termed cellular plasticity. Plasticity is not limited to in vitro manipulations but rather represents an important aspect of the regenerative response to injury in organs. Differentiated adult cells retain the capacity to dedifferentiate, adopting a progenitor-like phenotype after injury or, alternatively, to transdifferentiate, directly converting to a different mature cell type...
January 2017: Nature Reviews. Nephrology
Shikhar Aggarwal, Cristina Grange, Corinne Iampietro, Giovanni Camussi, Benedetta Bussolati
Persistent alterations of the renal tissue due to maladaptive repair characterize the outcome of acute kidney injury (AKI), despite a clinical recovery. Acute damage may also limit the renal production of erythropoietin, with impairment of the hemopoietic response to ischemia and possible lack of its reno-protective action. We aimed to evaluate the effect of a cell therapy using human CD133(+) renal progenitor cells on maladaptive repair and fibrosis following AKI in a model of glycerol-induced rhabdomyolysis...
November 17, 2016: Scientific Reports
Xiao-Ming Meng, Patrick Ming-Kuen Tang, Jun Li, Hui Yao Lan
BACKGROUND: Glomerular and interstitial macrophage infiltration is a feature for both the acute and chronic kidney diseases. Macrophages have been shown to play a diverse role in kidney injury and repair. Thus, macrophages may be a key cell type in acute and chronic kidney injury and repair. SUMMARY AND KEY MESSAGES: During renal inflammation, circulating monocytes are recruited and then become activated and polarized. By adapting to the local microenvironment, macrophages can differentiate into different phenotypes and function as a double-bladed sword in different stages of kidney disease...
September 2015: Kidney Diseases
Ana C de Bragança, Rildo A Volpini, Purvi Mehrotra, Lúcia Andrade, David P Basile
Reductions in renal microvasculature density and increased lymphocyte activity may play critical roles in the progression of chronic kidney disease (CKD) following acute kidney injury (AKI) induced by ischemia/reperfusion injury (IRI). Vitamin D deficiency is associated with tubulointerstitial damage and fibrosis progression following IRI-AKI We evaluated the effect of vitamin D deficiency in sustained IRI-AKI, hypothesizing that such deficiency contributes to the early reduction in renal capillary density or alters the lymphocyte response to IRI Wistar rats were fed vitamin D-free or standard diets for 35 days...
July 2016: Physiological Reports
Katherine Maringer, Sunder Sims-Lucas
Pediatric acute kidney injury (AKI) represents a complex disease process for clinicians as it is multifactorial in cause and only limited treatment or preventatives are available. The renal microvasculature has recently been implicated in AKI as a strong therapeutic candidate involved in both injury and recovery. Significant progress has been made in the ability to study the renal microvasculature following ischemic AKI and its role in repair. Advances have also been made in elucidating cell-cell interactions and the molecular mechanisms involved in these interactions...
August 2016: Pediatric Nephrology: Journal of the International Pediatric Nephrology Association
Andreas Linkermann
Acute tubular necrosis causes a loss of renal function, which clinically presents as acute kidney failure (AKI). The biochemical signaling pathways that trigger necrosis have been investigated in detail over the past 5 years. It is now clear that necrosis (regulated necrosis, RN) represents a genetically driven process that contributes to the pathophysiology of AKI. RN pathways such as necroptosis, ferroptosis, parthanatos, and mitochondrial permeability transition-induced regulated necrosis (MPT-RN) may be mechanistically distinct, and the relative contributions to overall organ damage during AKI in living organisms largely remain elusive...
January 2016: Kidney International
Jeffrey Rogers, Ravi Katari, Sheyna Gifford, Riccardo Tamburrini, Lauren Edgar, Marcia R Voigt, Sean V Murphy, Daniel Igel, Sara Mancone, Tyler Callese, Nicola Colucci, Majid Mirzazadeh, Andrea Peloso, Joao Paulo Zambon, Alan C Farney, Robert J Stratta, Giuseppe Orlando
Kidney transplantation (KT), as a modality of renal replacement therapy (RRT), has been shown to be both economically and functionally superior to dialysis for the treatment of end-stage renal disease (ESRD). Progress in KT is limited by two major barriers: a) a chronic and burgeoning shortage of transplantable organs and b) the need for chronic immunosuppression following transplantation. Although ground-breaking advances in transplant immunology have improved patient survival and graft durability, a new pathway of innovation is needed in order to overcome current obstacles...
2016: Expert Review of Clinical Immunology
Benjamin D Humphreys, Vincenzo Cantaluppi, Didier Portilla, Kai Singbartl, Li Yang, Mitchell H Rosner, John A Kellum, Claudio Ronco
AKI remains a highly prevalent disease associated with poor short- and long-term outcomes and high costs. Although significant advances in our understanding of repair after AKI have been made over the last 5 years, this knowledge has not yet been translated into new AKI therapies. A consensus conference held by the Acute Dialysis Quality Initiative was convened in April of 2014 and reviewed new evidence on successful kidney repair to identify the most promising pathways that could be translated into new treatments...
April 2016: Journal of the American Society of Nephrology: JASN
Sanjeev Kumar, Jing Liu, Paul Pang, A Michaela Krautzberger, Antoine Reginensi, Haruhiko Akiyama, Andreas Schedl, Benjamin D Humphreys, Andrew P McMahon
After acute kidney injury (AKI), surviving cells within the nephron proliferate and repair. We identify Sox9 as an acute epithelial stress response in renal regeneration. Translational profiling after AKI revealed a rapid upregulation of Sox9 within proximal tubule (PT) cells, the nephron cell type most vulnerable to AKI. Descendants of Sox9(+) cells generate the bulk of the nephron during development and regenerate functional PT epithelium after AKI-induced reactivation of Sox9 after renal injury. After restoration of renal function post-AKI, persistent Sox9 expression highlights regions of unresolved damage within injured nephrons...
August 25, 2015: Cell Reports
Jian Feng, Weiming Hu, Chunyue Feng, XiaoOu Mao, Kunlin Jin, Youxin Ye
The kidney is capable of regeneration following injury. However, whether renal stem/progenitor cells contribute to the repair process after injury, as well as the origin of the cells that repair and replace damaged renal tubule cells remains debated. Therefore, better understanding of the repair process will be critical to developing new strategies for the treatment of acute renal failure. Using an ischemia-reperfusion injury mode and an immunocytochemistry method, we counted the number of BrdU-positive cells in damged regions at different durations of reperfusion...
August 2015: Aging and Disease
Laura Lasagni, Maria Lucia Angelotti, Elisa Ronconi, Duccio Lombardi, Sara Nardi, Anna Peired, Francesca Becherucci, Benedetta Mazzinghi, Alessandro Sisti, Simone Romoli, Alexa Burger, Beat Schaefer, Annamaria Buccoliero, Elena Lazzeri, Paola Romagnani
Podocyte loss is a general mechanism of glomerular dysfunction that initiates and drives the progression of chronic kidney disease, which affects 10% of the world population. Here, we evaluate whether the regenerative response to podocyte injury influences chronic kidney disease outcome. In models of focal segmental glomerulosclerosis performed in inducible transgenic mice where podocytes are tagged, remission or progression of disease was determined by the amount of regenerated podocytes. When the same model was established in inducible transgenic mice where renal progenitors are tagged, the disease remitted if renal progenitors successfully differentiated into podocytes, while it persisted if differentiation was ineffective, resulting in glomerulosclerosis...
August 11, 2015: Stem Cell Reports
Joseph Fomusi Ndisang
The incidence of renal complications including kidney failure is on the rise. Moreover, with aging of the population and the high incidence of diabetes, hypertension and obesity, this trend may prevail. An important cytoprotective enzyme that has been shown to improve renal function is heme-oxygenase (HO). HO is known to abate apoptosis and necrosis, and improves cell vitality, which in turn, may enhance tissue regeneration. Consistently, HO has been shown to restore tissue morphology by potentiating potentiate proteins of repair/regeneration and promoting neovascularization...
2015: Current Pharmaceutical Design
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