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Semin Nephrol. 2019 Jan;39(1):96-106. doi: 10.1016/j.semnephrol.2018.10.007.

Kidney-Immune System Crosstalk in AKI.

Author information

1
Department of Critical Care Medicine, Mayo Clinic, Phoenix, AZ; Center for Critical Care Nephrology, Department of Critical Care Medicine, University of Pittsburgh, Pittsburgh, PA. Electronic address: ks.ms@posteo.de.
2
Center for Critical Care Nephrology, Department of Critical Care Medicine, University of Pittsburgh, Pittsburgh, PA.

Abstract

Acute kidney injury (AKI) now is recognized as a systemic disease. It occurs frequently in critically ill patients and has profound effects on morbidity and mortality. Recent research efforts have shown a bidirectional interplay between AKI and the immune system. Both innate and adaptive immune responses mediate renal injury as well as recovery from AKI. Dendritic cells, monocytes/macrophages, neutrophils, T lymphocytes, and B lymphocytes all play specific roles in the development of AKI. M2 macrophages and regulatory T cells also are pivotal in controlling inflammation, tissue remodeling, and repair after AKI. Conversely, existing evidence also suggests that increased production and decreased clearance of cytokines as well as dysfunction of immune cells, in particular neutrophils, can contribute to immune dysfunction and impaired bacterial clearance during AKI. Clinical data indicate that AKI is a risk factor for infections after various forms of critical illness, including cardiac surgery, malignancies, or severe trauma. Available evidence does not suggest that standard renal replacement therapies improve outcome from AKI beyond control of fluid balance and azotemia. Thus, novel approaches likely will be necessary to prevent or treat AKI-induced dysregulation of the inflammatory response.

KEYWORDS:

Acute kidney injury; infection; inflammation

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