Discovery and validation of cell cycle arrest biomarkers in human acute kidney injury
Introduction Acute kidney injury (AKI) can evolve quickly and clinical measures of function often fail to detect AKI at a time when interventions are likely to provide benefit. Identifying early markers of kidney damage has been difficult due to the complex nature of human AKI, in which multiple eti...
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| Veröffentlicht in: | Critical care (London, England) Jg. 17; H. 1; S. R25 |
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| Hauptverfasser: | , , , , , , , , , , , , , , , , , , , , , , , , , , , , , , , , , , , , , , , , |
| Format: | Journal Article |
| Sprache: | Englisch |
| Veröffentlicht: |
London
BioMed Central
06.02.2013
BioMed Central Ltd |
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| ISSN: | 1364-8535, 1466-609X, 1364-8535, 1466-609X |
| Online-Zugang: | Volltext |
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| Abstract | Introduction
Acute kidney injury (AKI) can evolve quickly and clinical measures of function often fail to detect AKI at a time when interventions are likely to provide benefit. Identifying early markers of kidney damage has been difficult due to the complex nature of human AKI, in which multiple etiologies exist. The objective of this study was to identify and validate novel biomarkers of AKI.
Methods
We performed two multicenter observational studies in critically ill patients at risk for AKI - discovery and validation. The top two markers from discovery were validated in a second study (Sapphire) and compared to a number of previously described biomarkers. In the discovery phase, we enrolled 522 adults in three distinct cohorts including patients with sepsis, shock, major surgery, and trauma and examined over 300 markers. In the Sapphire validation study, we enrolled 744 adult subjects with critical illness and without evidence of AKI at enrollment; the final analysis cohort was a heterogeneous sample of 728 critically ill patients. The primary endpoint was moderate to severe AKI (KDIGO stage 2 to 3) within 12 hours of sample collection.
Results
Moderate to severe AKI occurred in 14% of Sapphire subjects. The two top biomarkers from discovery were validated. Urine insulin-like growth factor-binding protein 7 (IGFBP7) and tissue inhibitor of metalloproteinases-2 (TIMP-2), both inducers of G
1
cell cycle arrest, a key mechanism implicated in AKI, together demonstrated an AUC of 0.80 (0.76 and 0.79 alone). Urine [TIMP-2]
·
[IGFBP7] was significantly superior to all previously described markers of AKI (
P
<0.002), none of which achieved an AUC >0.72. Furthermore, [TIMP-2]
·
[IGFBP7] significantly improved risk stratification when added to a nine-variable clinical model when analyzed using Cox proportional hazards model, generalized estimating equation, integrated discrimination improvement or net reclassification improvement. Finally, in sensitivity analyses [TIMP-2]
·
[IGFBP7] remained significant and superior to all other markers regardless of changes in reference creatinine method.
Conclusions
Two novel markers for AKI have been identified and validated in independent multicenter cohorts. Both markers are superior to existing markers, provide additional information over clinical variables and add mechanistic insight into AKI.
Trial registration
ClinicalTrials.gov number
NCT01209169
. |
|---|---|
| AbstractList | Acute kidney injury (AKI) can evolve quickly and clinical measures of function often fail to detect AKI at a time when interventions are likely to provide benefit. Identifying early markers of kidney damage has been difficult due to the complex nature of human AKI, in which multiple etiologies exist. The objective of this study was to identify and validate novel biomarkers of AKI.
We performed two multicenter observational studies in critically ill patients at risk for AKI - discovery and validation. The top two markers from discovery were validated in a second study (Sapphire) and compared to a number of previously described biomarkers. In the discovery phase, we enrolled 522 adults in three distinct cohorts including patients with sepsis, shock, major surgery, and trauma and examined over 300 markers. In the Sapphire validation study, we enrolled 744 adult subjects with critical illness and without evidence of AKI at enrollment; the final analysis cohort was a heterogeneous sample of 728 critically ill patients. The primary endpoint was moderate to severe AKI (KDIGO stage 2 to 3) within 12 hours of sample collection.
Moderate to severe AKI occurred in 14% of Sapphire subjects. The two top biomarkers from discovery were validated. Urine insulin-like growth factor-binding protein 7 (IGFBP7) and tissue inhibitor of metalloproteinases-2 (TIMP-2), both inducers of G1 cell cycle arrest, a key mechanism implicated in AKI, together demonstrated an AUC of 0.80 (0.76 and 0.79 alone). Urine [TIMP-2]·[IGFBP7] was significantly superior to all previously described markers of AKI (P <0.002), none of which achieved an AUC >0.72. Furthermore, [TIMP-2]·[IGFBP7] significantly improved risk stratification when added to a nine-variable clinical model when analyzed using Cox proportional hazards model, generalized estimating equation, integrated discrimination improvement or net reclassification improvement. Finally, in sensitivity analyses [TIMP-2]·[IGFBP7] remained significant and superior to all other markers regardless of changes in reference creatinine method.
Two novel markers for AKI have been identified and validated in independent multicenter cohorts. Both markers are superior to existing markers, provide additional information over clinical variables and add mechanistic insight into AKI.
ClinicalTrials.gov number NCT01209169. Introduction Acute kidney injury (AKI) can evolve quickly and clinical measures of function often fail to detect AKI at a time when interventions are likely to provide benefit. Identifying early markers of kidney damage has been difficult due to the complex nature of human AKI, in which multiple etiologies exist. The objective of this study was to identify and validate novel biomarkers of AKI. Methods We performed two multicenter observational studies in critically ill patients at risk for AKI - discovery and validation. The top two markers from discovery were validated in a second study (Sapphire) and compared to a number of previously described biomarkers. In the discovery phase, we enrolled 522 adults in three distinct cohorts including patients with sepsis, shock, major surgery, and trauma and examined over 300 markers. In the Sapphire validation study, we enrolled 744 adult subjects with critical illness and without evidence of AKI at enrollment; the final analysis cohort was a heterogeneous sample of 728 critically ill patients. The primary endpoint was moderate to severe AKI (KDIGO stage 2 to 3) within 12 hours of sample collection. Results Moderate to severe AKI occurred in 14% of Sapphire subjects. The two top biomarkers from discovery were validated. Urine insulin-like growth factor-binding protein 7 (IGFBP7) and tissue inhibitor of metalloproteinases-2 (TIMP-2), both inducers of G 1 cell cycle arrest, a key mechanism implicated in AKI, together demonstrated an AUC of 0.80 (0.76 and 0.79 alone). Urine [TIMP-2] · [IGFBP7] was significantly superior to all previously described markers of AKI ( P <0.002), none of which achieved an AUC >0.72. Furthermore, [TIMP-2] · [IGFBP7] significantly improved risk stratification when added to a nine-variable clinical model when analyzed using Cox proportional hazards model, generalized estimating equation, integrated discrimination improvement or net reclassification improvement. Finally, in sensitivity analyses [TIMP-2] · [IGFBP7] remained significant and superior to all other markers regardless of changes in reference creatinine method. Conclusions Two novel markers for AKI have been identified and validated in independent multicenter cohorts. Both markers are superior to existing markers, provide additional information over clinical variables and add mechanistic insight into AKI. Trial registration ClinicalTrials.gov number NCT01209169 . Introduction Acute kidney injury (AKI) can evolve quickly and clinical measures of function often fail to detect AKI at a time when interventions are likely to provide benefit. Identifying early markers of kidney damage has been difficult due to the complex nature of human AKI, in which multiple etiologies exist. The objective of this study was to identify and validate novel biomarkers of AKI. Methods We performed two multicenter observational studies in critically ill patients at risk for AKI - discovery and validation. The top two markers from discovery were validated in a second study (Sapphire) and compared to a number of previously described biomarkers. In the discovery phase, we enrolled 522 adults in three distinct cohorts including patients with sepsis, shock, major surgery, and trauma and examined over 300 markers. In the Sapphire validation study, we enrolled 744 adult subjects with critical illness and without evidence of AKI at enrollment; the final analysis cohort was a heterogeneous sample of 728 critically ill patients. The primary endpoint was moderate to severe AKI (KDIGO stage 2 to 3) within 12 hours of sample collection. Results Moderate to severe AKI occurred in 14% of Sapphire subjects. The two top biomarkers from discovery were validated. Urine insulin-like growth factor-binding protein 7 (IGFBP7) and tissue inhibitor of metalloproteinases-2 (TIMP-2), both inducers of G.sub.1 cell cycle arrest, a key mechanism implicated in AKI, together demonstrated an AUC of 0.80 (0.76 and 0.79 alone). Urine [TIMP-2]*[IGFBP7] was significantly superior to all previously described markers of AKI (P <0.002), none of which achieved an AUC >0.72. Furthermore, [TIMP-2]*[IGFBP7] significantly improved risk stratification when added to a nine-variable clinical model when analyzed using Cox proportional hazards model, generalized estimating equation, integrated discrimination improvement or net reclassification improvement. Finally, in sensitivity analyses [TIMP-2]*[IGFBP7] remained significant and superior to all other markers regardless of changes in reference creatinine method. Conclusions Two novel markers for AKI have been identified and validated in independent multicenter cohorts. Both markers are superior to existing markers, provide additional information over clinical variables and add mechanistic insight into AKI. Trial registration ClinicalTrials.gov number NCT01209169. Acute kidney injury (AKI) can evolve quickly and clinical measures of function often fail to detect AKI at a time when interventions are likely to provide benefit. Identifying early markers of kidney damage has been difficult due to the complex nature of human AKI, in which multiple etiologies exist. The objective of this study was to identify and validate novel biomarkers of AKI.INTRODUCTIONAcute kidney injury (AKI) can evolve quickly and clinical measures of function often fail to detect AKI at a time when interventions are likely to provide benefit. Identifying early markers of kidney damage has been difficult due to the complex nature of human AKI, in which multiple etiologies exist. The objective of this study was to identify and validate novel biomarkers of AKI.We performed two multicenter observational studies in critically ill patients at risk for AKI - discovery and validation. The top two markers from discovery were validated in a second study (Sapphire) and compared to a number of previously described biomarkers. In the discovery phase, we enrolled 522 adults in three distinct cohorts including patients with sepsis, shock, major surgery, and trauma and examined over 300 markers. In the Sapphire validation study, we enrolled 744 adult subjects with critical illness and without evidence of AKI at enrollment; the final analysis cohort was a heterogeneous sample of 728 critically ill patients. The primary endpoint was moderate to severe AKI (KDIGO stage 2 to 3) within 12 hours of sample collection.METHODSWe performed two multicenter observational studies in critically ill patients at risk for AKI - discovery and validation. The top two markers from discovery were validated in a second study (Sapphire) and compared to a number of previously described biomarkers. In the discovery phase, we enrolled 522 adults in three distinct cohorts including patients with sepsis, shock, major surgery, and trauma and examined over 300 markers. In the Sapphire validation study, we enrolled 744 adult subjects with critical illness and without evidence of AKI at enrollment; the final analysis cohort was a heterogeneous sample of 728 critically ill patients. The primary endpoint was moderate to severe AKI (KDIGO stage 2 to 3) within 12 hours of sample collection.Moderate to severe AKI occurred in 14% of Sapphire subjects. The two top biomarkers from discovery were validated. Urine insulin-like growth factor-binding protein 7 (IGFBP7) and tissue inhibitor of metalloproteinases-2 (TIMP-2), both inducers of G1 cell cycle arrest, a key mechanism implicated in AKI, together demonstrated an AUC of 0.80 (0.76 and 0.79 alone). Urine [TIMP-2]·[IGFBP7] was significantly superior to all previously described markers of AKI (P <0.002), none of which achieved an AUC >0.72. Furthermore, [TIMP-2]·[IGFBP7] significantly improved risk stratification when added to a nine-variable clinical model when analyzed using Cox proportional hazards model, generalized estimating equation, integrated discrimination improvement or net reclassification improvement. Finally, in sensitivity analyses [TIMP-2]·[IGFBP7] remained significant and superior to all other markers regardless of changes in reference creatinine method.RESULTSModerate to severe AKI occurred in 14% of Sapphire subjects. The two top biomarkers from discovery were validated. Urine insulin-like growth factor-binding protein 7 (IGFBP7) and tissue inhibitor of metalloproteinases-2 (TIMP-2), both inducers of G1 cell cycle arrest, a key mechanism implicated in AKI, together demonstrated an AUC of 0.80 (0.76 and 0.79 alone). Urine [TIMP-2]·[IGFBP7] was significantly superior to all previously described markers of AKI (P <0.002), none of which achieved an AUC >0.72. Furthermore, [TIMP-2]·[IGFBP7] significantly improved risk stratification when added to a nine-variable clinical model when analyzed using Cox proportional hazards model, generalized estimating equation, integrated discrimination improvement or net reclassification improvement. Finally, in sensitivity analyses [TIMP-2]·[IGFBP7] remained significant and superior to all other markers regardless of changes in reference creatinine method.Two novel markers for AKI have been identified and validated in independent multicenter cohorts. Both markers are superior to existing markers, provide additional information over clinical variables and add mechanistic insight into AKI.CONCLUSIONSTwo novel markers for AKI have been identified and validated in independent multicenter cohorts. Both markers are superior to existing markers, provide additional information over clinical variables and add mechanistic insight into AKI.ClinicalTrials.gov number NCT01209169.TRIAL REGISTRATIONClinicalTrials.gov number NCT01209169. Acute kidney injury (AKI) can evolve quickly and clinical measures of function often fail to detect AKI at a time when interventions are likely to provide benefit. Identifying early markers of kidney damage has been difficult due to the complex nature of human AKI, in which multiple etiologies exist. The objective of this study was to identify and validate novel biomarkers of AKI. We performed two multicenter observational studies in critically ill patients at risk for AKI - discovery and validation. The top two markers from discovery were validated in a second study (Sapphire) and compared to a number of previously described biomarkers. In the discovery phase, we enrolled 522 adults in three distinct cohorts including patients with sepsis, shock, major surgery, and trauma and examined over 300 markers. In the Sapphire validation study, we enrolled 744 adult subjects with critical illness and without evidence of AKI at enrollment; the final analysis cohort was a heterogeneous sample of 728 critically ill patients. The primary endpoint was moderate to severe AKI (KDIGO stage 2 to 3) within 12 hours of sample collection. Moderate to severe AKI occurred in 14% of Sapphire subjects. The two top biomarkers from discovery were validated. Urine insulin-like growth factor-binding protein 7 (IGFBP7) and tissue inhibitor of metalloproteinases-2 (TIMP-2), both inducers of G.sub.1 cell cycle arrest, a key mechanism implicated in AKI, together demonstrated an AUC of 0.80 (0.76 and 0.79 alone). Urine [TIMP-2]*[IGFBP7] was significantly superior to all previously described markers of AKI (P <0.002), none of which achieved an AUC >0.72. Furthermore, [TIMP-2]*[IGFBP7] significantly improved risk stratification when added to a nine-variable clinical model when analyzed using Cox proportional hazards model, generalized estimating equation, integrated discrimination improvement or net reclassification improvement. Finally, in sensitivity analyses [TIMP-2]*[IGFBP7] remained significant and superior to all other markers regardless of changes in reference creatinine method. Two novel markers for AKI have been identified and validated in independent multicenter cohorts. Both markers are superior to existing markers, provide additional information over clinical variables and add mechanistic insight into AKI. |
| ArticleNumber | R25 |
| Audience | Academic |
| Author | Joannes-Boyau, Olivier Joannidis, Michael Vinsonneau, Christophe Kim, Patrick Honore, Patrick M Kellum, John A Marx, Gernot Wagner, Ludwig Rimmelé, Thomas Birkhahn, Robert Bihorac, Azra Vincent, Jean-Louis Zacharowski, Kai Lissauer, Matthew E Wilkerson, R Gentry Kashani, Kianoush Laskowitz, Daniel T Haase, Michael Hoste, Eric AJ Artigas, Antonio Walker, Michael G Al-Khafaji, Ali Mullaney, Scott McCullough, Peter A Sprague, Amy M Cely, Cynthia M Forni, Lui G Gunnerson, Kyle J Ardiles, Thomas Hackett, James Bell, Max Koyner, Jay L Ostermann, Marlies Shapiro, Nathan I Shaw, Andrew D Shi, Jing Bagshaw, Sean M Feldkamp, Thorsten Davison, Danielle L Gong, Michelle Ng Chawla, Lakhmir S |
| AuthorAffiliation | 2 Department of Critical Care Medicine, University of Pittsburgh School of Medicine, 3550 Terrace Street, Pittsburgh, PA 15213, USA 17 ICU Department, Universitair Ziekenhuis Brussel (UZB), Vrije Universiteit Brussel (VUB), Laarbeeklaan 101, Brussels 1090, Belgium 7 Department of Anesthesiology, University of Florida, 1660 SW Archer Road, Gainesville, FL 32611, USA 13 Department of Medicine, Montefiore Medical Center, Albert Einstein College of Medicine, 111 East 210th Street, Bronx, NY 10467, USA 3 Department of Critical Care, Maricopa Integrated Health System, 2601 E Roosevelt Street, Phoenix, AZ 85008, USA 30 Department of Emergency Medicine, Beth Israel Deaconess Medical Center, 1 Deaconess Road, Boston, MA 2215, USA 26 Department of Medicine, St John Providence Health System, Providence Hospitals and Medical Centers, Providence Park Heart Institute, 47601 Grand River Avenue, Novi, MI 48374, USA 34 Department of Intensive Care, Erasme University Hospital, Route De Lennik 808, Brussels, 10 |
| AuthorAffiliation_xml | – name: 4 Critical Care Center, Sabadell Hospital, CIBER Enfermedades Respiratorias, Autonomous University of Barcelona, Parc Tauli s/n, Sabadell, Barcelona 8208, Spain – name: 12 Intensive Care Medicine, Western Sussex Hospitals Trust, Lyndhurst Road, Worthing, West Sussex, BN11 2DH, UK – name: 9 Bruce W. Carter Department of Veterans Affairs Medical Center, 1201 NW 16th Street, Miami, FL 33125, USA – name: 16 Hackett & Associates, Inc., 14419 Rancho Del Prado Trail, San Diego, CA 92127, USA – name: 24 Department of Surgery, University of Maryland School of Medicine, 22 South Greene Street, Baltimore, MD 21201, USA – name: 36 Department of Internal Medicine, Medical University of Vienna, Spitalgasse 23, Vienna 1090, Austria – name: 20 Department of Internal Medicine, ICU, Medical University Innsbruck, Anichstrasse 35, Innsbruck, A-6020, Austria – name: 33 Department of Medicine, Joseph M. Still Research Foundation, 3675 J. Dewey Gray Circle, Augusta, GA 30909, USA – name: 38 Clinic of Anesthesiology, Intensive Care Medicine and Pain Therapy, University Hospital Frankfurt, Theodor-Stern-Kai 7, Frankfurt am Main, 60590, Germany – name: 10 Department of Anesthesiology and Critical Care Medicine, George Washington University Medical Center, 900 23rd Street NW, Washington, DC 20037, USA – name: 22 Department of Medicine, University of Chicago, 6030 South Ellis Avenue, Chicago, IL 60637, USA – name: 23 Department of Medicine, Duke University Medical Center, 2301 Erwin Road, Durham, NC 27710, USA – name: 6 Department of Anesthesia and Intensive Care Medicine, Karolinska University Hospital, Karolinskavagen, Solna, Stockholm SE-171 76, Sweden – name: 25 Department of Intensive Care, Universitätsklinikum der RWTH Aachen, Pauwelsstrasse 30, Aachen, 52074, Germany – name: 31 Department of Anesthesia, Duke University Medical Center/Durham Veterans Affairs Medical Center, 508 Fulton Street, Durham, NC 27705, USA – name: 7 Department of Anesthesiology, University of Florida, 1660 SW Archer Road, Gainesville, FL 32611, USA – name: 19 Anaesthesiology and Critical Care Department 2, University Hospital of Bordeaux, 1 Avenue De Magellon, Pessac, 33600, France – name: 34 Department of Intensive Care, Erasme University Hospital, Route De Lennik 808, Brussels, 1070, Belgium – name: 11 Department of Nephrology, University Hospital Essen, University Duisburg-Essen, Hufelandstrasse 55, Essen, 45147, Germany – name: 35 Department of Intensive Care, Hospital Marc Jacquet, 2 Rue Freteau De Peny, Melun, 77011, France – name: 17 ICU Department, Universitair Ziekenhuis Brussel (UZB), Vrije Universiteit Brussel (VUB), Laarbeeklaan 101, Brussels 1090, Belgium – name: 27 Department of Medicine, University of California San Diego, 200 West Arbor Drive, San Diego, CA 92103, USA – name: 21 Traumatology, Surgical Critical Care and Emergency Surgery, Hospital of the University of Pennsylvania, 3400 Spruce Street, Philadelphia, PA 19104, USA – name: 26 Department of Medicine, St John Providence Health System, Providence Hospitals and Medical Centers, Providence Park Heart Institute, 47601 Grand River Avenue, Novi, MI 48374, USA – name: 15 Department of Nephrology, Otto-von-Guericke-Universitat Magdeburg, Leipziger Strasse 44, Magdeburg, 39120, Germany – name: 5 Division of Critical Care Medicine, Faculty of Medicine and Dentistry, University of Alberta, 3C1.12 Walter C. Mackenzie Centre, 8440 112 Street NW, Edmonton, Alberta T6G 2B7, Canada – name: 30 Department of Emergency Medicine, Beth Israel Deaconess Medical Center, 1 Deaconess Road, Boston, MA 2215, USA – name: 39 Department of Critical Care Medicine, University of Pittsburgh, School of Medicine, 3550 Terrace Street, Pittsburgh, PA 15213, USA – name: 29 Service D'Anesthésie Réanimation, Edouard Herriot Hospital, Hospices civils de Lyon, 5 Place d'Arsonval, Lyon, 69003, France – name: 1 Division of Pulmonary and Critical Care Medicine, Mayo Clinic, 200 First Street SW, Rochester, MN 55905, USA – name: 18 Intensive Care Unit, Ghent University Hospital, De Pintelaan 185, Ghent, 9000, Belgium – name: 14 Departments of Anesthesiology and Emergency Medicine, Virginia Commonwealth University Medical Center, 1200 East Broad Street, Richmond, VA 23298, USA – name: 13 Department of Medicine, Montefiore Medical Center, Albert Einstein College of Medicine, 111 East 210th Street, Bronx, NY 10467, USA – name: 28 Department of Critical Care, King's College London, Guy's and St Thomas' Hospital, Westminster Bridge Road, London, SE1 7EH, UK – name: 8 Department of Emergency Medicine, New York Methodist Hospital, 506 6th Street, Brooklyn, NY 11215, USA – name: 2 Department of Critical Care Medicine, University of Pittsburgh School of Medicine, 3550 Terrace Street, Pittsburgh, PA 15213, USA – name: 3 Department of Critical Care, Maricopa Integrated Health System, 2601 E Roosevelt Street, Phoenix, AZ 85008, USA – name: 37 Department of Emergency Medicine, Tampa General Hospital, 1 Davis Boulevard, Tampa, FL 33606, USA – name: 32 Walker Biosciences, 6321 Allston Street, Carlsbad, CA 92009, USA |
| Author_xml | – sequence: 1 givenname: Kianoush surname: Kashani fullname: Kashani, Kianoush organization: Division of Pulmonary and Critical Care Medicine, Mayo Clinic – sequence: 2 givenname: Ali surname: Al-Khafaji fullname: Al-Khafaji, Ali organization: Department of Critical Care Medicine, University of Pittsburgh School of Medicine – sequence: 3 givenname: Thomas surname: Ardiles fullname: Ardiles, Thomas organization: Department of Critical Care, Maricopa Integrated Health System – sequence: 4 givenname: Antonio surname: Artigas fullname: Artigas, Antonio organization: Critical Care Center, Sabadell Hospital, CIBER Enfermedades Respiratorias,Parc Tauli s/n, Autonomous University of Barcelona – sequence: 5 givenname: Sean M surname: Bagshaw fullname: Bagshaw, Sean M organization: Division of Critical Care Medicine, Faculty of Medicine and Dentistry, University of Alberta – sequence: 6 givenname: Max surname: Bell fullname: Bell, Max organization: Department of Anesthesia and Intensive Care Medicine, Karolinska University Hospital – sequence: 7 givenname: Azra surname: Bihorac fullname: Bihorac, Azra organization: Department of Anesthesiology, University of Florida – sequence: 8 givenname: Robert surname: Birkhahn fullname: Birkhahn, Robert organization: Department of Emergency Medicine, New York Methodist Hospital – sequence: 9 givenname: Cynthia M surname: Cely fullname: Cely, Cynthia M organization: Bruce W. Carter Department of Veterans Affairs Medical Center – sequence: 10 givenname: Lakhmir S surname: Chawla fullname: Chawla, Lakhmir S organization: Department of Anesthesiology and Critical Care Medicine, George Washington University Medical Center – sequence: 11 givenname: Danielle L surname: Davison fullname: Davison, Danielle L organization: Department of Anesthesiology and Critical Care Medicine, George Washington University Medical Center – sequence: 12 givenname: Thorsten surname: Feldkamp fullname: Feldkamp, Thorsten organization: Department of Nephrology, University Hospital Essen, University Duisburg-Essen – sequence: 13 givenname: Lui G surname: Forni fullname: Forni, Lui G organization: Intensive Care Medicine, Western Sussex Hospitals Trust – sequence: 14 givenname: Michelle Ng surname: Gong fullname: Gong, Michelle Ng organization: Department of Medicine, Montefiore Medical Center, Albert Einstein College of Medicine – sequence: 15 givenname: Kyle J surname: Gunnerson fullname: Gunnerson, Kyle J organization: Departments of Anesthesiology and Emergency Medicine, Virginia Commonwealth University Medical Center – sequence: 16 givenname: Michael surname: Haase fullname: Haase, Michael organization: Department of Nephrology, Otto-von-Guericke-Universitat Magdeburg – sequence: 17 givenname: James surname: Hackett fullname: Hackett, James organization: Hackett Associates, Inc – sequence: 18 givenname: Patrick M surname: Honore fullname: Honore, Patrick M organization: ICU Department, Universitair Ziekenhuis Brussel (UZB), Vrije Universiteit Brussel (VUB) – sequence: 19 givenname: Eric AJ surname: Hoste fullname: Hoste, Eric AJ organization: Intensive Care Unit, Ghent University Hospital – sequence: 20 givenname: Olivier surname: Joannes-Boyau fullname: Joannes-Boyau, Olivier organization: Anaesthesiology and Critical Care Department 2, University Hospital of Bordeaux – sequence: 21 givenname: Michael surname: Joannidis fullname: Joannidis, Michael organization: Department of Internal Medicine, ICU, Medical University Innsbruck – sequence: 22 givenname: Patrick surname: Kim fullname: Kim, Patrick organization: Traumatology, Surgical Critical Care and Emergency Surgery, Hospital of the University of Pennsylvania – sequence: 23 givenname: Jay L surname: Koyner fullname: Koyner, Jay L organization: Department of Medicine, University of Chicago – sequence: 24 givenname: Daniel T surname: Laskowitz fullname: Laskowitz, Daniel T organization: Department of Medicine, Duke University Medical Center – sequence: 25 givenname: Matthew E surname: Lissauer fullname: Lissauer, Matthew E organization: Department of Surgery, University of Maryland School of Medicine – sequence: 26 givenname: Gernot surname: Marx fullname: Marx, Gernot organization: Department of Intensive Care, Universitätsklinikum der RWTH Aachen – sequence: 27 givenname: Peter A surname: McCullough fullname: McCullough, Peter A organization: Department of Medicine, St John Providence Health System, Providence Hospitals and Medical Centers, Providence Park Heart Institute – sequence: 28 givenname: Scott surname: Mullaney fullname: Mullaney, Scott organization: Department of Medicine, University of California San Diego – sequence: 29 givenname: Marlies surname: Ostermann fullname: Ostermann, Marlies organization: Department of Critical Care, King's College London, Guy's and St Thomas' Hospital – sequence: 30 givenname: Thomas surname: Rimmelé fullname: Rimmelé, Thomas organization: Service D'Anesthésie Réanimation, Edouard Herriot Hospital, Hospices civils de Lyon – sequence: 31 givenname: Nathan I surname: Shapiro fullname: Shapiro, Nathan I organization: Department of Emergency Medicine, Beth Israel Deaconess Medical Center – sequence: 32 givenname: Andrew D surname: Shaw fullname: Shaw, Andrew D organization: Department of Anesthesia, Duke University Medical Center/Durham Veterans Affairs Medical Center – sequence: 33 givenname: Jing surname: Shi fullname: Shi, Jing organization: Walker Biosciences – sequence: 34 givenname: Amy M surname: Sprague fullname: Sprague, Amy M organization: Department of Medicine, Joseph M. Still Research Foundation – sequence: 35 givenname: Jean-Louis surname: Vincent fullname: Vincent, Jean-Louis organization: Department of Intensive Care, Erasme University Hospital – sequence: 36 givenname: Christophe surname: Vinsonneau fullname: Vinsonneau, Christophe organization: Department of Intensive Care, Hospital Marc Jacquet – sequence: 37 givenname: Ludwig surname: Wagner fullname: Wagner, Ludwig organization: Department of Internal Medicine, Medical University of Vienna – sequence: 38 givenname: Michael G surname: Walker fullname: Walker, Michael G organization: Walker Biosciences – sequence: 39 givenname: R Gentry surname: Wilkerson fullname: Wilkerson, R Gentry organization: Department of Emergency Medicine, Tampa General Hospital – sequence: 40 givenname: Kai surname: Zacharowski fullname: Zacharowski, Kai organization: Clinic of Anesthesiology, Intensive Care Medicine and Pain Therapy, University Hospital Frankfurt – sequence: 41 givenname: John A surname: Kellum fullname: Kellum, John A email: kellumja@ccm.upmc.edu organization: Department of Critical Care Medicine, University of Pittsburgh, School of Medicine |
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Acute kidney injury (AKI) can evolve quickly and clinical measures of function often fail to detect AKI at a time when interventions are likely to... Acute kidney injury (AKI) can evolve quickly and clinical measures of function often fail to detect AKI at a time when interventions are likely to provide... Introduction Acute kidney injury (AKI) can evolve quickly and clinical measures of function often fail to detect AKI at a time when interventions are likely to... |
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| SubjectTerms | Acute Kidney Injury - diagnosis Acute Kidney Injury - urine Acute renal failure Aged Biological markers Biomarkers - urine Cell cycle Cell Cycle Checkpoints - physiology Cohort Studies Comparative analysis Critical Care Medicine Emergency Medicine Female Humans Insulin-Like Growth Factor Binding Proteins - urine Intensive Male Medical research Medicine Medicine & Public Health Medicine, Experimental Middle Aged Pharmaceutical industry Physiological aspects Protein binding Tissue Inhibitor of Metalloproteinase-2 - urine |
| Title | Discovery and validation of cell cycle arrest biomarkers in human acute kidney injury |
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