Nsaids and Kidney
. Update Article
NSAIDs and Kidney
P Ejaz, K Bhojani, VR Joshi*
Abstract
NSAIDs are commonly used drugs. Even with the advent of selective COX-2 inhibitors, nephrotoxicity still remains a concern. The adverse effects of NSAIDs are mediated via inhibition of prostaglandin synthesis from arachidonic acid by non-specific blocking of the enzyme cyclooxygenase leading to vasoconstriction and reversible mild renal impairment in volume contracted states. When unopposed, this may lead to acute tubular necrosis and acute renal failure. NSAIDs also produce interstitial nephritis with or without nephrotic syndrome secondary to minimal change disease. Although this presents as acute renal failure, it can progress in some cases to chronic renal failure. Papillary necrosis has been incriminated in the development of chronic renal failure secondary to NSAIDs. In patients on long term NSAIDs without acute or chronic renal failure, subclinical renal dysfunction such as reduced creatinine clearance and impaired urine concentrating ability has been shown to be present. Although this sub-clinical dysfunction is reversible on withdrawal of NSAIDs, some reports have suggested a persistent residual dysfunction. Even with a wide range of NSAIDs at our disposal, a renal safe NSAID is yet to be discovered. ©
INTRODUCTION on steroidal anti-inflammatory drugs (NSAIDs) are amongst the most commonly prescribed medication. Some are available over the counter and likely to be abused. Serious gastrointestinal side effects have been minimized with the advent of selective and specific COX-2 inhibitors and misoprostol. However, the newer NSAIDs continue to be nephrotoxic much like the conventional NSAIDs.1 Nephrotoxicity attributed to NSAIDS has been reviewed in the past.2-8 The spectrum of nephrotoxicity includes acute tubular necrosis, acute tubulointerstitial nephritis, glomerulonephritis, renal papillary necrosis, chronic renal failure, salt and water retention, hypertension,
NSAIDs and Kidney
P Ejaz, K Bhojani, VR Joshi*
Abstract
NSAIDs are commonly used drugs. Even with the advent of selective COX-2 inhibitors, nephrotoxicity still remains a concern. The adverse effects of NSAIDs are mediated via inhibition of prostaglandin synthesis from arachidonic acid by non-specific blocking of the enzyme cyclooxygenase leading to vasoconstriction and reversible mild renal impairment in volume contracted states. When unopposed, this may lead to acute tubular necrosis and acute renal failure. NSAIDs also produce interstitial nephritis with or without nephrotic syndrome secondary to minimal change disease. Although this presents as acute renal failure, it can progress in some cases to chronic renal failure. Papillary necrosis has been incriminated in the development of chronic renal failure secondary to NSAIDs. In patients on long term NSAIDs without acute or chronic renal failure, subclinical renal dysfunction such as reduced creatinine clearance and impaired urine concentrating ability has been shown to be present. Although this sub-clinical dysfunction is reversible on withdrawal of NSAIDs, some reports have suggested a persistent residual dysfunction. Even with a wide range of NSAIDs at our disposal, a renal safe NSAID is yet to be discovered. ©
INTRODUCTION on steroidal anti-inflammatory drugs (NSAIDs) are amongst the most commonly prescribed medication. Some are available over the counter and likely to be abused. Serious gastrointestinal side effects have been minimized with the advent of selective and specific COX-2 inhibitors and misoprostol. However, the newer NSAIDs continue to be nephrotoxic much like the conventional NSAIDs.1 Nephrotoxicity attributed to NSAIDS has been reviewed in the past.2-8 The spectrum of nephrotoxicity includes acute tubular necrosis, acute tubulointerstitial nephritis, glomerulonephritis, renal papillary necrosis, chronic renal failure, salt and water retention, hypertension,