Abstract
Introduction: Despite advancements in renal replacement therapy, acute kidney injury (AKI) harbors a grave prognosis, likely due to extra-renal organ dysfunction. Kidney ischemia-reperfusion injury (IRI) activates cellular and soluble mediators that incite a distinct distant pulmonary transcriptional response in vivo, leading to TNFR1-dependent pulmonary apoptosis, increased microvascular permeability and lung injury. Hypothesizing that pulmonary endothelial cell (EC) structural changes could result in lung microvascular barrier dysfunction in vivo, we performed phenotypic assessment of cytoskeletal derangements, apoptosis, and pathway-focused genomic analyses of candidate genes to characterize in vitro pulmonary EC-specific changes during kidney IRI.
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