Abstract

NVESTIGATIONS on the role of eicosanoids in immune-mediated renal injury have spanned more than a decade and continue to provide new knowledge on the importance of these lipid compounds in the pathophysiology of various forms of renal immune injury, such as glomerulonephritis, lupus nephritis, and kidney allograft rejection. There is now ample evidence to implicate specific eicosanoids in participating in a number of pathobiological processes known to occur in immune-mediated renal injury that can result in end-stage renal failure, if allowed to progress. Table 1 outlines these processes and correlates them with specific eicosanoids that have been shown to play a regulatory role in each process. 1-24 It is apparent that specific eicosanoids can be linked to one or more processes, such as renal hemodynamic impairment, cellular proliferation, or extracellular matrix synthesis. Because it is now feasible to effectively and selectively inhibit the synthesis or action of specific eicosanoids, investigations to define the role of eicosanoids in mediating these processes in renal immune injury hold promise in that the information accrued can lead to new therapeutic strategies to treat patients with various forms of immune-mediated renal injury, which remains a most frequent cause of end-stage renal failure. Indeed, a wealth of information has become available from such investigations and is reviewed in this article.

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