Non-steroidal anti-inflammatory drugs ( NSAIDs, including COX-2 inhibitors ) may rarely precipitate renal failure, and vulnerable ( particularly elderly ) patients may be at increased risk. NSAID use accounts for an estimated 15% of all cases of drug-induced acute renal failure.

A case-control study estimated an increased relative risk ( 3.2 ) of acute renal failure in otherwise healthy current users of NSAIDs.

MHRA ( Medicines and Healthcare products Regulatory Agency ) is continuing to receive case reports of renal failure in NSAID users.

Prescribing information for NSAIDs includes warnings about renal impairment and renal failure, and advises that the risk of renal failure is highest in those with existing renal impairment.
In patients with conditions that cause renal hypoperfusion, prostaglandin production may be increased to maintain adequate renal blood flow. The adverse renal effects associated with NSAIDs are mainly mediated via inhibition of prostaglandin-induced vasodilation and can result in reduced renal blood flow. Patients with conditions such as hypovolaemia, congestive heart failure, liver cirrhosis, or multiple myeloma are at particular risk.

Contributing risk factors include the current administration of medicines such as angiotensin converting enzyme ( Ace ) inhibitors, angiotensin II receptors antagonists, and diuretics.

NSAIDs may also produce direct toxic effects on the kidney. The main mechanisms for acute renal failure include acute tubular necrosis and acute interstitial nephritis. Other rarer mechanisms have also been reported, such as acute papillary necrosis and renal vasculitis. Adverse renal effects are generally reversible on discontinuation of NSAID treatment.

Source: Drug Safety Update – MHRA, 2009

XagenaMedicine2009


Link: Xapedia - Medical Encyclopedia