A review of the role of immune cells in acute kidney injury

Anthony Bonavia, Kai Singbartl

Research output: Contribution to journalReview article

21 Citations (Scopus)

Abstract

Acute kidney injury (AKI) is a systemic disease occurring commonly in patients who are critically ill. Etiologies of AKI can be septic or aseptic (nephrotoxic, or ischemia–reperfusion injury). Recent evidence reveals that innate and adaptive immune responses are involved in mediating damage to renal tubular cells and in recovery from AKI. Dendritic cells, monocytes/macrophages, neutrophils, T lymphocytes, and B lymphocytes all contribute to kidney injury. Conversely, M2 macrophages and regulatory T cells are essential in suppressing inflammation, tissue remodeling and repair following kidney injury. AKI itself confers an increased risk for developing infection owing to increased production and decreased clearance of cytokines, in addition to dysfunction of immune cells themselves. Neutrophils are the predominant cell type rendered dysfunctional by AKI. In this review, we describe the bi-directional interplay between the immune system and AKI and summarize recent developments in this field of research.

Original languageEnglish (US)
Pages (from-to)1629-1639
Number of pages11
JournalPediatric Nephrology
Volume33
Issue number10
DOIs
StatePublished - Oct 1 2018

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Acute Kidney Injury
Kidney
Wounds and Injuries
Neutrophils
Macrophages
Adaptive Immunity
Regulatory T-Lymphocytes
Innate Immunity
Critical Illness
Dendritic Cells
Monocytes
Immune System
B-Lymphocytes
Cytokines
Inflammation
T-Lymphocytes
Infection
Research

All Science Journal Classification (ASJC) codes

  • Pediatrics, Perinatology, and Child Health
  • Nephrology

Cite this

Bonavia, Anthony ; Singbartl, Kai. / A review of the role of immune cells in acute kidney injury. In: Pediatric Nephrology. 2018 ; Vol. 33, No. 10. pp. 1629-1639.
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A review of the role of immune cells in acute kidney injury. / Bonavia, Anthony; Singbartl, Kai.

In: Pediatric Nephrology, Vol. 33, No. 10, 01.10.2018, p. 1629-1639.

Research output: Contribution to journalReview article

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