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Kidney Week

Abstract: PO0193

Microparticles Containing M2 Monocyte and Other Inflammatory Markers Are Released in AKI

Session Information

  • AKI Mechanisms - 2
    October 22, 2020 | Location: On-Demand
    Abstract Time: 10:00 AM - 12:00 PM

Category: Acute Kidney Injury

  • 103 AKI: Mechanisms

Authors

  • Campos, Begoña, University of Cincinnati College of Medicine, Cincinnati, Ohio, United States
  • Harrison, Kathleen, University of Cincinnati College of Medicine, Cincinnati, Ohio, United States
  • Kramer, Samantha M., University of Cincinnati College of Medicine, Cincinnati, Ohio, United States
  • Abu Jawdeh, Bassam G., University of Cincinnati College of Medicine, Cincinnati, Ohio, United States
  • Thakar, Charuhas V., University of Cincinnati College of Medicine, Cincinnati, Ohio, United States
Background

Renal epithelial cell injury in AKI and induces a pleiotropic inflammatory cell response. Monocyte phenotypes (M1 = CD14+/CD16-; M2 = CD14+/CD16+), and subsequently derived tissue-resident macrophages play a critical role in inflammation and repair in acute kidney injury (AKI). It is accepted that M1 phenotype serves a pro-inflammatory/phagocytic role, whereas M2 phenotype influences tissue repair and remodelling. We have previously shown that microparticles (MP) derived from renal epithelial cells are released in the setting of kidney injury and can be detected in vitro as well as in human plasma, and can carry the biological activity.

Methods

In this study, we evaluated presence of MP expressing markers of inflammation in AKI (defined by standardized criteria). Human samples were derived from a prospectively collected repository (31 cases of AKI in critically ill patients compared to 22 living kidney donor healthy controls). Samples were prepared to measure MP (standard methods), and flow cytometric analysis was evaluated using antibodies against inflammatory proteins. FlowJo software was used for analysis. Mann-Whitney test was used for comparisons.

Results

The average age was 54 years; mean admission creatinine was 1.8 mg/dl, and the time between admission and sample collection was 3-4 days.
MP containing M2 Monocyte markers were significantly higher in AKI patients compared to controls (347.03 vs 271.36 /ml respectively; p=0.02). MP containing M1 markers were similar compared to control (177.85 vs 285.40 /ml, p=0.19), AKI cases also showed significantly higher levels of MP containing other inflammatory markers: Leukocytes (CD45, p=0.015), eosinophils (CD66b, p=0.0001), and also in platelets (CD42b, p=0.05).

Conclusion

MP containing monocyte/macrophage markers of M2 phenotype are released in the early phase of AKI, which can influence tissue modelling and repair. Moreover, a pattern of MP representing markers of M2 and other inflammatory cells may have prognostic significance to predict the severity of tissue injury or the prospect of recovery.