Various mechanisms, for instance hypertension, heart failure, renal failure and increased tendency for thrombosis have been proposed to explain an increased risk with COX-2 selective NSAIDs, with emphasis on their considerable inhibition of prostacyclin synthesis but failure to inhibit COX-1-mediated generation of thromboxane A2 in platelets (which are devoid of COX-2) [15], [16], [17], [18], [19], [20]. Here, PTGS2 is linked to acute kidney injury.