Eicosanoids and Platelet Activating Factor as Possible Mediators of Injury in Experimental Nephropathies

  • Giuseppe Remuzzi
Part of the Advances in Experimental Medicine and Biology book series (AEMB, volume 259)

Abstract

That secondary mediators of inflammation such as arachidonate (AA) metabolites and platelet activating factor (PAF) determine morphological and clinical expression of toxic or immune-mediated nephropathies has been the subject of extensive investigations in the last few years. More recently the demonstration that, beside circulating inflammatory cells, resident renal cells can generate prostaglandins and thromboxane A2 (TxA2) (1,2) as well as PAF (3) has opened new perspectives to clarify the mechanisms of tissue damage in the above-mentioned conditions. Most interestingly, both AA metabolites and PAF may have a common precursor (4,5), and both can be formed as a consequence of phospholipase A2 activation (6,7). Thus, a new field of investigation in renal diseases will be to clarify the relation between the two pathways as determinant of tissue injury.

Keywords

Permeability Angiotensin Macromolecule Cardiol Indomethacin 

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Copyright information

© Plenum Press, New York 1989

Authors and Affiliations

  • Giuseppe Remuzzi
    • 1
    • 2
  1. 1.Mario Negri Institute for Pharmacological ResearchBergamoItaly
  2. 2.Division of Nephrology and DialysisOspedali Riuniti de BergamoItaly

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