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Kidney Int. 2017 Jan;91(1):45-60. doi: 10.1016/j.kint.2016.07.032. Epub 2016 Sep 28.

Renal perfusion in sepsis: from macro- to microcirculation.

Author information

1
Department of Intensive Care, Erasme University Hospital, Université Libre de Bruxelles, Brussels, Belgium.
2
Center for Critical Care Nephrology, Department of Critical Care Medicine, University of Pittsburgh, Pittsburgh, Pennsylvania, USA.
3
Centre for Integrated Critical Care, School of Medicine, The University of Melbourne, Parkville, Melbourne, Australia.
4
Department of Intensive Care, Erasme University Hospital, Université Libre de Bruxelles, Brussels, Belgium. Electronic address: jlvincent@intensive.org.

Abstract

The pathogenesis of sepsis-associated acute kidney injury is complex and likely involves perfusion alterations, a dysregulated inflammatory response, and bioenergetic derangements. Although global renal hypoperfusion has been the main target of therapeutic interventions, its role in the development of renal dysfunction in sepsis is controversial. The implications of renal hypoperfusion during sepsis probably extend beyond a simple decrease in glomerular filtration pressure, and targeting microvascular perfusion deficits to maintain tubular epithelial integrity and function may be equally important. In this review, we provide an overview of macro- and microcirculatory dysfunction in experimental and clinical sepsis and discuss relationships with kidney oxygenation, metabolism, inflammation, and function.

KEYWORDS:

acute kidney injury; renal hypoperfusion; sepsis

PMID:
27692561
DOI:
10.1016/j.kint.2016.07.032
[Indexed for MEDLINE]

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