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Prostanoids generated by the metabolism of arachidonic acid through the cyclooxygenase (COX) pathway have diverse functions in health and disease.1 The kidney is prominent among the physiologic systems affected by these ubiquitous mediators. Along with effects to modulate renal blood flow, GFR, and sodium excretion, prostanoids affect the function of the glomerular filtration barrier. This is illustrated by clinical studies showing that nonsteroidal anti-inflammatory drugs (NSAIDs), which inhibit COX enzymes, attenuate the levels of proteinuria in patients with glomerular diseases.2,3 Because NSAIDs block production of all prostanoids, the specific prostanoids influencing glomerular function in this setting cannot be discerned. Moreover, because NSAIDs frequently cause adverse effects in patients with kidney disease, including acute deterioration in GFR and exacerbation of hypertension, this approach to antiproteinuric therapy has limited applications.In experimental models of glomerular disease, a number of studies have indicated beneficial effects of more specific pharmacologic inhibitors that block individual prostanoid synthetic pathways or receptors. More recently, this issue has been explored using modern molecular genetics. For example, Harris and associates4,5 showed that overexpression of the inducible COX isoform, COX2, in podocytes of transgenic mice enhances susceptibility to glomerular injury caused by adriamycin or puromycin. This was due, at least in part, to exaggerated production of thromboxane A2 and activation of the thromboxane-prostanoid (TP) receptor.6 These findings are consistent with older studies showing efficacy of …

The EP4 Receptor for Prostaglandin E2 in Glomerular Disease