Renal damage induced by non-steroidal anti-inflammatory drug treatment

Abstract Non-steroidal anti-inflammatory drugs (NSAIDs) are extensively used worldwide due to their analgesic, antipyretic and antiinflammatory effects. NSAIDs (both non-selective NSAIDs and selective cyclooxygenase-2 inhibitors) have nephrotoxic potential, particularly when used chronically.The principal mechanism of action of NSAIDs is cyclooxygenase inhibition, which prevents the conversion of arachidonic acid to prostaglandins, prostacyclins and thromboxanes. In the kidney, prostaglandins induce vasodilation and counter the action of the renin-angiotensin-aldosterone system and the sympathetic nervous system, ensuring optimal renal perfusion. Inhibition of this mechanism by NSAIDs can result in renal damage: acute kidney injury through hemodynamic mechanism, acute interstitial nephritis, glomerular disease, papillary necrosis, water and electrolyte imbalances, HTN. Chronic NSAID use may lead to chronic kidney disease.The nephrotoxic effect is reduced in young patients without renal disease or other comorbidities, but increases significantly in elderly patients with pre-existing kidney disease, nephrotic syndrome, diabetes mellitus, severe congestive heart failure, volume depletion, cirrhosis with ascites, HTN, atherosclerosis, or in patients under treatment with diuretics, angiotensin-converting enzyme inhibitors, angiotensin receptor inhibitors.