Renal perfusion in sepsis: from macro- to microcirculation

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


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.

Publication types

  • Review

MeSH terms

  • Acute Kidney Injury / etiology*
  • Animals
  • Clinical Trials as Topic
  • Glomerular Filtration Rate
  • Humans
  • Kidney / blood supply*
  • Kidney / metabolism
  • Microcirculation*
  • Nitric Oxide / metabolism
  • Nitric Oxide Synthase Type II / metabolism
  • Nitric Oxide Synthase Type III / metabolism
  • Reactive Oxygen Species / metabolism
  • Renal Circulation*
  • Sepsis / complications*
  • Sepsis / microbiology


  • Reactive Oxygen Species
  • Nitric Oxide
  • Nitric Oxide Synthase Type II
  • Nitric Oxide Synthase Type III