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AKI Repair

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By Isabel Acosta-Ochoa Nephrology senior staff. Valladolid. Spain
Katja Berger, Marcus J Moeller
Acute kidney injury (AKI) is a common clinical problem and is associated with high mortality rates. It is accepted that after AKI cellular regeneration of the proximal tubule occurs from intrinsic tubule cells. Recently, scattered tubular cells (STCs) were discovered as a novel subpopulation of tubule cells involved in regeneration. STCs have a distinct morphology, unique protein expression profile resembling that of parietal epithelial cells, proliferate more than the remaining proximal tubule cells, and are less susceptible to injuries...
July 2014: Seminars in Nephrology
Elena Lazzeri, Maria Lucia Angelotti, Anna Peired, Carolina Conte, Julian A Marschner, Laura Maggi, Benedetta Mazzinghi, Duccio Lombardi, Maria Elena Melica, Sara Nardi, Elisa Ronconi, Alessandro Sisti, Giulia Antonelli, Francesca Becherucci, Letizia De Chiara, Ricardo Romero Guevara, Alexa Burger, Beat Schaefer, Francesco Annunziato, Hans-Joachim Anders, Laura Lasagni, Paola Romagnani
Acute kidney injury (AKI) is considered largely reversible based on the capacity of surviving tubular cells to dedifferentiate and replace lost cells via cell division. Here we show by tracking individual tubular cells in conditional Pax8/Confetti mice that kidney function is  recovered after AKI despite substantial tubular cell loss. Cell cycle and ploidy analysis upon AKI in conditional Pax8/FUCCI2aR mice and human biopsies identify endocycle-mediated hypertrophy of tubular cells. By contrast, a small subset of Pax2+ tubular progenitors enriches via higher stress resistance and clonal expansion and regenerates necrotic tubule segments, a process that can be enhanced by suitable drugs...
April 9, 2018: Nature Communications
Dong Zhou, Haiyan Fu, Liangxiang Xiao, Hongyan Mo, Hui Zhuo, Xiaojun Tian, Lin Lin, Jianhua Xing, Youhua Liu
AKI is a devastating condition with high morbidity and mortality. The pathologic features of AKI are characterized by tubular injury, inflammation, and vascular impairment. Whether fibroblasts in the renal interstitium have a role in the pathogenesis of AKI is unknown. In this study, we investigated the role of fibroblast-specific β -catenin signaling in dictating the outcome of AKI, using conditional knockout mice in which β -catenin was specifically ablated in fibroblasts (Gli1- β -cat-/-). After ischemia-reperfusion injury (IRI), Gli1- β -cat-/- mice had lower serum creatinine levels and less morphologic injury than Gli1- β -cat+/+ littermate controls...
January 17, 2018: Journal of the American Society of Nephrology: JASN
Sanjeev Kumar
The acutely injured mammalian kidney mounts a cellular and molecular response to repair itself. However, in patchy regions such intrinsic processes are impaired and dysregulated leading to chronic kidney disease. Currently, no therapy exists to treat established acute kidney injury per se. Strategies to augment human endogenous repair processes and retard associated profibrotic responses are urgently required. Recent studies have identified injury-induced activation of the intrinsic molecular driver of epithelial regeneration and induction of partial epithelial to the mesenchymal state, respectively...
January 2018: Kidney International
Rohan Datta, Ada Wong, Troy Camarata, Farhana Tamanna, Imran Ilahi, Aleksandr Vasilyev
Acute Kidney Injury (AKI) is a common medical condition with a high mortality rate. With the repair abilities of the kidney, it is possible to restore adequate kidney function after supportive treatment. However, a better understanding of how nephron cell death and repair occur on the cellular level is required to minimize cell death and to enhance the regenerative process. The zebrafish pronephros is a good model system to accomplish this goal because it contains anatomical segments that are similar to the mammalian nephron...
June 3, 2017: Journal of Visualized Experiments: JoVE
Sul A Lee, Sanjeev Noel, Mohanraj Sadasivam, Abdel R A Hamad, Hamid Rabb
Acute kidney injury (AKI) is a significant problem in both native and transplant kidneys. There have been significant advances in understanding the role of immune cells in the early injury and repair from AKI. In this brief review, we aim to update information on the pathophysiologic impact of various immune cells in AKI, with special emphasis on repair. An improved understanding of the AKI immunopathology will lead to new therapies that prevent AKI, accelerate repair, and prevent the progression of AKI to chronic kidney disease...
June 10, 2017: Nephron
Yutian Lei, Hans-Joachim Anders
Evolutionary medicine has proven helpful to understand the origin of human disease, e.g. in identifying causal roles of recent environmental changes impacting on human physiology (environment-phenotype mismatch). In contrast, diseases affecting only a limited number of members of a species often originate from evolutionary trade-offs for usually physiologic adaptations assuring reproductive success in the context of extrinsic threats. For example, the G1 and G2 variants of the APOL1 gene supporting control of Trypanosoma infection come with the trade-off that they promote the progression of kidney disease...
May 8, 2017: Histology and Histopathology
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 (~100 nm 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...
June 1, 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...
December 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
2015-12-09 11:17:40
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