Abstract
Abstract
An upregulation of arachidonate metabolism often accompanies renal pathophysiologic states. The resulting eicosanoids contribute to, or modify, the underlying process. Recent investigations suggest that platelet-neutrophil interactions, as well as alterations in the expression of the inducible isoform of cyclooxygenase, play a critical role in mediating changes in arachidonate metabolism in renal inflammation. The importance of arachidonate to renal pathophysiology has been highlighted by prior investigations which have demonstrated a beneficial effect of dietary polyunsaturated fatty acid (PUFA) modulation in a variety of models of experimental renal disease. More recent work has established that this beneficial effect may depend upon alterations in both lipid mediator generation as well as changes in cell function. In light of the benefits of dietary PUFA modulation in models of experimental renal disease, there have been numerous recent clinical trials of dietary (n-3) PUFA supplementation in patients with a variety of renal disorders. These clinical trials suggest that such therapy may be an important addition to the clinical armamentarium, especially in the treatment of IgA nephropathy
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