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Semin Nephrol. 2015 Jan;35(1):64-74. doi: 10.1016/j.semnephrol.2015.01.007.

Sepsis-associated acute kidney injury: macrohemodynamic and microhemodynamic alterations in the renal circulation.

Author information

1
Adult Critical Care Unit, Department of Renal Medicine and Transplantation, The Royal London Hospital, Barts Health NHS Trust, London, UK; William Harvey Research Institute, Queen Mary University of London, London, UK.
2
Department of Intensive Care, Austin Hospital, Melbourne, Australia; Australian and New Zealand Intensive Care Research Centre, Department of Epidemiology and Preventive Medicine, Monash University, Melbourne, Australia. Electronic address: rinaldo.bellomo@austin.org.au.

Abstract

Traditionally, renal ischemia has been regarded as central to the pathogenesis of sepsis-associated acute kidney injury (SA-AKI). Accordingly, hemodynamic management of SA-AKI has emphasized restoration of renal perfusion, whereas, experimentally, ischemia reperfusion models have been emphasized. However, in human beings, SA-AKI usually is accompanied by hyperdynamic circulation. Moreover, clinical and experimental evidence now suggests the importance of inflammatory mechanisms in the development of AKI and microcirculatory dysfunction more than systemic alteration in renal perfusion. In this review, we examine systemic, regional, and microcirculatory hemodynamics in SA-AKI, and attempt to rationalize the hemodynamic management of this condition.

KEYWORDS:

Acute kidney injury; critical care; hemodynamic management; microcirculation; renal blood flow; sepsis

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