Arachidonic acid metabolites are suspected of contributing in various ways to major pathophysiological events that occur in toxic and immune glomerular injury. This paper focuses on the role of arachidonate metabolites in the experimental models of adriamycin nephrosis and cyclosporin A nephrotoxicity in rats as examples, respectively, of a toxic nephropathy characterized by increased glomerular permeability to proteins and a toxic nephropathy with macrophage accumulation and progressively deteriorating renal function. The important pathogenic contribution of thromboxane A2 to the impairment of renal function in these experimental models is discussed.