Cyclooxygenase enzymes expression in the kidney

Abstract

Chronic kidney disease (CKD) is one of a common cause of death in both human and animals. Persistent proteinuria of renal origin and systemic hypertension are clinical and biological findings that are usually associated with more progressive kidney disease. In human medicine, renal cyclooxygenase (COX) enzymes (especially COX-2) have been involved in the progression of CKD as one of the biological mechanism that modulates hypertension and/or proteinuria via their products, prostanoids. Furthermore, COX-2 has been proposed to play a pathophysiological role in experimental models of progressive renal injury. However, inhibition of COX enzyme activity by non-steroidal anti-inflammatory drugs (NSAIDs), when used in clinical practice to provide pain relief and anti-inflammatory effects, can lead to renal adverse effects. This is because the prostanoids generated by renal COX enzymes have important physiological roles in the kidney.