What is it about?
Acute kidney injury, as currently clinically defined, is caused by a heterogeneous set of pathophysiologic processes and is associated with variable outcomes. It is unknown if this heterogeneity can be parsed into clinical sub-phenotypes with differing underlying biology, risk for clinical outcomes and response to therapies. This study identified two novel AKI sub-phenotypes independently in two critically ill populations. To ease future sub-phenotype identification, a three-variable model was developed. This model was applied to patients in the Vasopressin in Septic Shock (VASST) clinical trial and the identified AKI sub-phenotypes had a differential response to the addition of vasopressin relative to norepinephrine therapy. Identification of AKI sub-phenotypes could improve risk prognostication and may be useful for predictive enrichment, whereby a patient’s AKI sub-phenotype status could inform vasopressor response.
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This page is a summary of: Identification of Acute Kidney Injury Subphenotypes with Differing Molecular Signatures and Responses to Vasopressin Therapy, American Review of Respiratory Disease, April 2019, American Thoracic Society,
DOI: 10.1164/rccm.201807-1346oc.
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