Abstract
Arachidonic acid (AA) metabolites are produced by a variety of renal cells, although the eicosanoid profile varies among different cell types and regions of the kidney. The details of eicosanoid biosynthesis and metabolism are discussed in a preceding chapter. The importance of arachidonic acid metabolites in renal disease has emerged from experimental studies and clinical evaluation of immunologically mediated, as well as non-immune, forms of renal injury. Since arachidonic acid metabolites (eicosanoids), in particular thromboxane (TxA2), prostacyclin (PGI2), prostaglandin E2 (PGE2) and leukotri-enes (LT), can regulate haemodynamic and immunological/inflammatory events, an alteration in the metabolism of any of these molecules can promote or protect the formation of renal injury.
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