Endotoxemia, renal hypoperfusion, and fever: interactive risk factors for aminoglycoside and sepsis-associated acute renal failure

Am J Kidney Dis. 1992 Sep;20(3):223-30. doi: 10.1016/s0272-6386(12)80694-9.


Sepsis and aminoglycoside administration remain leading causes of clinical acute renal failure (ARF). In recent years, a number of experimental studies from different laboratories have indicated that specific components of the septic state, most notably fever, endotoxemia, and renal hypoperfusion, can interact to induce synergistic renal damage, acting in concert to produce acute tubular necrosis and ARF. If sepsis-associated ARF has a multifactorial basis, then a number of interventions directed at one or more of its etiologic components could confer protection. In this brief review, evidence to support these pathophysiological and therapeutic considerations are presented.

Publication types

  • Research Support, U.S. Gov't, P.H.S.
  • Review

MeSH terms

  • Acute Kidney Injury / epidemiology
  • Acute Kidney Injury / etiology*
  • Aminoglycosides
  • Animals
  • Anti-Bacterial Agents / adverse effects*
  • Endotoxins / adverse effects*
  • Fever / complications*
  • Gram-Negative Bacterial Infections / complications*
  • Gram-Negative Bacterial Infections / drug therapy
  • Humans
  • Kidney / blood supply*
  • Kidney Tubular Necrosis, Acute / epidemiology
  • Kidney Tubular Necrosis, Acute / etiology*
  • Risk Factors


  • Aminoglycosides
  • Anti-Bacterial Agents
  • Endotoxins