Precision management of acute kidney injury in the intensive care unit: current state of the art

Acute kidney injury (AKI) is a prototypical example of a common syndrome in critical illness defined by consensus. The consensus definition for AKI, traditionally defined using only serum creatinine and urine output, was needed to standardize the description for epidemiology and to harmonize eligibi...

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Veröffentlicht in:Intensive care medicine Jg. 49; H. 9; S. 1049 - 1061
Hauptverfasser: Stanski, Natalja L., Rodrigues, Camila E., Strader, Michael, Murray, Patrick T., Endre, Zoltan H., Bagshaw, Sean M.
Format: Journal Article
Sprache:Englisch
Veröffentlicht: Berlin/Heidelberg Springer Berlin Heidelberg 01.09.2023
Springer
Springer Nature B.V
Schlagworte:
Anesthesiology
Biomarkers
Clinical trials
Creatinine
Critical Care Medicine
Emergency Medicine
Epidemiology
Gelatinase
Genetic aspects
Growth factors
Health services
Illnesses
Injuries
Intensive
Intensive care
Kidneys
Leukocytes (neutrophilic)
Lipocalin
Medical colleges
Medical prognosis
Medicine
Medicine & Public Health
Olfactomedin
Pain Medicine
Patients
Pediatrics
Phenotypes
Pneumology/Respiratory System
Precision medicine
Protein binding
Renin
Review
Tissue inhibitor of metalloproteinase 2
Enrichment
Biomarker
Phenotype
Prognosis
Precision
Acute kidney injury
Endotype
ISSN:0342-4642, 1432-1238, 1432-1238
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Abstract Acute kidney injury (AKI) is a prototypical example of a common syndrome in critical illness defined by consensus. The consensus definition for AKI, traditionally defined using only serum creatinine and urine output, was needed to standardize the description for epidemiology and to harmonize eligibility for clinical trials. However, AKI is not a simple disease, but rather a complex and multi-factorial syndrome characterized by a wide spectrum of pathobiology. AKI is now recognized to be comprised of numerous sub-phenotypes that can be discriminated through shared features such as etiology, prognosis, or common pathobiological mechanisms of injury and damage. The characterization of sub-phenotypes can serve to enable prognostic enrichment (i.e., identify subsets of patients more likely to share an outcome of interest) and predictive enrichment (identify subsets of patients more likely to respond favorably to a given therapy). Existing and emerging biomarkers will aid in discriminating sub-phenotypes of AKI, facilitate expansion of diagnostic criteria, and be leveraged to realize personalized approaches to management, particularly for recognizing treatment-responsive mechanisms (i.e., endotypes) and targets for intervention (i.e., treatable traits). Specific biomarkers (e.g., serum renin; olfactomedin 4 (OLFM4); interleukin (IL)-9) may further enable identification of pathobiological mechanisms to serve as treatment targets. However, even non-specific biomarkers of kidney injury (e.g., neutrophil gelatinase-associated lipocalin, NGAL; [tissue inhibitor of metalloproteinases 2, TIMP2]·[insulin like growth factor binding protein 7, IGFBP7]; kidney injury molecule 1, KIM-1) can direct greater precision management for specific sub-phenotypes of AKI. This review will summarize these evolving concepts and recent innovations in precision medicine approaches to the syndrome of AKI in critical illness, along with providing examples of how they can be leveraged to guide patient care.
AbstractList Acute kidney injury (AKI) is a prototypical example of a common syndrome in critical illness defined by consensus. The consensus definition for AKI, traditionally defined using only serum creatinine and urine output, was needed to standardize the description for epidemiology and to harmonize eligibility for clinical trials. However, AKI is not a simple disease, but rather a complex and multi-factorial syndrome characterized by a wide spectrum of pathobiology. AKI is now recognized to be comprised of numerous sub-phenotypes that can be discriminated through shared features such as etiology, prognosis, or common pathobiological mechanisms of injury and damage. The characterization of sub-phenotypes can serve to enable prognostic enrichment (i.e., identify subsets of patients more likely to share an outcome of interest) and predictive enrichment (identify subsets of patients more likely to respond favorably to a given therapy). Existing and emerging biomarkers will aid in discriminating sub-phenotypes of AKI, facilitate expansion of diagnostic criteria, and be leveraged to realize personalized approaches to management, particularly for recognizing treatment-responsive mechanisms (i.e., endotypes) and targets for intervention (i.e., treatable traits). Specific biomarkers (e.g., serum renin; olfactomedin 4 (OLFM4); interleukin (IL)-9) may further enable identification of pathobiological mechanisms to serve as treatment targets. However, even non-specific biomarkers of kidney injury (e.g., neutrophil gelatinase-associated lipocalin, NGAL; [tissue inhibitor of metalloproteinases 2, TIMP2]·[insulin like growth factor binding protein 7, IGFBP7]; kidney injury molecule 1, KIM-1) can direct greater precision management for specific sub-phenotypes of AKI. This review will summarize these evolving concepts and recent innovations in precision medicine approaches to the syndrome of AKI in critical illness, along with providing examples of how they can be leveraged to guide patient care.Acute kidney injury (AKI) is a prototypical example of a common syndrome in critical illness defined by consensus. The consensus definition for AKI, traditionally defined using only serum creatinine and urine output, was needed to standardize the description for epidemiology and to harmonize eligibility for clinical trials. However, AKI is not a simple disease, but rather a complex and multi-factorial syndrome characterized by a wide spectrum of pathobiology. AKI is now recognized to be comprised of numerous sub-phenotypes that can be discriminated through shared features such as etiology, prognosis, or common pathobiological mechanisms of injury and damage. The characterization of sub-phenotypes can serve to enable prognostic enrichment (i.e., identify subsets of patients more likely to share an outcome of interest) and predictive enrichment (identify subsets of patients more likely to respond favorably to a given therapy). Existing and emerging biomarkers will aid in discriminating sub-phenotypes of AKI, facilitate expansion of diagnostic criteria, and be leveraged to realize personalized approaches to management, particularly for recognizing treatment-responsive mechanisms (i.e., endotypes) and targets for intervention (i.e., treatable traits). Specific biomarkers (e.g., serum renin; olfactomedin 4 (OLFM4); interleukin (IL)-9) may further enable identification of pathobiological mechanisms to serve as treatment targets. However, even non-specific biomarkers of kidney injury (e.g., neutrophil gelatinase-associated lipocalin, NGAL; [tissue inhibitor of metalloproteinases 2, TIMP2]·[insulin like growth factor binding protein 7, IGFBP7]; kidney injury molecule 1, KIM-1) can direct greater precision management for specific sub-phenotypes of AKI. This review will summarize these evolving concepts and recent innovations in precision medicine approaches to the syndrome of AKI in critical illness, along with providing examples of how they can be leveraged to guide patient care.
Acute kidney injury (AKI) is a prototypical example of a common syndrome in critical illness defined by consensus. The consensus definition for AKI, traditionally defined using only serum creatinine and urine output, was needed to standardize the description for epidemiology and to harmonize eligibility for clinical trials. However, AKI is not a simple disease, but rather a complex and multi-factorial syndrome characterized by a wide spectrum of pathobiology. AKI is now recognized to be comprised of numerous sub-phenotypes that can be discriminated through shared features such as etiology, prognosis, or common pathobiological mechanisms of injury and damage. The characterization of sub-phenotypes can serve to enable prognostic enrichment (i.e., identify subsets of patients more likely to share an outcome of interest) and predictive enrichment (identify subsets of patients more likely to respond favorably to a given therapy). Existing and emerging biomarkers will aid in discriminating sub-phenotypes of AKI, facilitate expansion of diagnostic criteria, and be leveraged to realize personalized approaches to management, particularly for recognizing treatment-responsive mechanisms (i.e., endotypes) and targets for intervention (i.e., treatable traits). Specific biomarkers (e.g., serum renin; olfactomedin 4 (OLFM4); interleukin (IL)-9) may further enable identification of pathobiological mechanisms to serve as treatment targets. However, even non-specific biomarkers of kidney injury (e.g., neutrophil gelatinase-associated lipocalin, NGAL; [tissue inhibitor of metalloproteinases 2, TIMP2]·[insulin like growth factor binding protein 7, IGFBP7]; kidney injury molecule 1, KIM-1) can direct greater precision management for specific sub-phenotypes of AKI. This review will summarize these evolving concepts and recent innovations in precision medicine approaches to the syndrome of AKI in critical illness, along with providing examples of how they can be leveraged to guide patient care.
Audience Academic
Author Murray, Patrick T.
Stanski, Natalja L.
Rodrigues, Camila E.
Bagshaw, Sean M.
Strader, Michael
Endre, Zoltan H.
Author_xml – sequence: 1
  givenname: Natalja L.
  orcidid: 0000-0003-4473-8376
  surname: Stanski
  fullname: Stanski, Natalja L.
  organization: Division of Critical Care Medicine, Cincinnati Children’s Hospital Medical Center
– sequence: 2
  givenname: Camila E.
  orcidid: 0000-0003-0562-0893
  surname: Rodrigues
  fullname: Rodrigues, Camila E.
  organization: Department of Nephrology, Prince of Wales Clinical School, UNSW Medicine, Nephrology Department, Hospital das Clínicas, University of São Paulo School of Medicine
– sequence: 3
  givenname: Michael
  orcidid: 0000-0002-5089-8539
  surname: Strader
  fullname: Strader, Michael
  organization: Department of Medicine, School of Medicine, University College Dublin
– sequence: 4
  givenname: Patrick T.
  orcidid: 0000-0001-8516-1839
  surname: Murray
  fullname: Murray, Patrick T.
  organization: Department of Medicine, School of Medicine, University College Dublin
– sequence: 5
  givenname: Zoltan H.
  surname: Endre
  fullname: Endre, Zoltan H.
  organization: Department of Nephrology, Prince of Wales Clinical School, UNSW Medicine
– sequence: 6
  givenname: Sean M.
  orcidid: 0000-0003-3633-6596
  surname: Bagshaw
  fullname: Bagshaw, Sean M.
  email: bagshaw@ualberta.ca
  organization: Department of Critical Care Medicine, Faculty of Medicine and Dentistry, University of Alberta and Alberta Health Services
BackLink https://www.ncbi.nlm.nih.gov/pubmed/37552332$$D View this record in MEDLINE/PubMed
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Issue 9
Keywords Enrichment
Biomarker
Phenotype
Prognosis
Precision
Acute kidney injury
Endotype
Language English
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SubjectTerms Anesthesiology
Biomarkers
Clinical trials
Creatinine
Critical Care Medicine
Emergency Medicine
Epidemiology
Gelatinase
Genetic aspects
Growth factors
Health services
Illnesses
Injuries
Intensive
Intensive care
Kidneys
Leukocytes (neutrophilic)
Lipocalin
Medical colleges
Medical prognosis
Medicine
Medicine & Public Health
Olfactomedin
Pain Medicine
Patients
Pediatrics
Phenotypes
Pneumology/Respiratory System
Precision medicine
Protein binding
Renin
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Tissue inhibitor of metalloproteinase 2
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Title Precision management of acute kidney injury in the intensive care unit: current state of the art
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