Analgesic Nephrotoxicity
10. What are the risks of analgesic nephropathy from NSAID use in E.T.?
Analgesic overuse is a common cause of chronic interstitial nephritis (CIN) and may account for approximately 5% of the cases of chronic renal failure in the United States. Historically, aspirin and phenacetin in combination were thought to be the causative agent for most cases of CIN; however, acetaminophen, aspirin,67 and other NSAIDs68,69 also have been implicated. Acetaminophen-induced renal toxicity is almost always accompanied by concomitant serum hepatic transaminase changes and generally is associated with acute acetaminophen intoxication.70 Most cases of interstitial nephritis seem to be related to both dose and duration of NSAID therapy.71,72 (Also see Chapter 30, Acute Renal Failure.)
The NSAID's effect on renal function may be twofold. NSAIDs can directly damage renal tubules and can also reduce renal blood flow by inhibiting prostacyclin. Prostacyclin modifies renal function in response to the effects of endogenous vasoconstrictors (e.g., norepinephrine and angiotensin II), especially if the patient is volume depleted, has been taking diuretics, or is elderly. Renal insufficiency may occur in 20% of patients with one or more of these identifiable risks who also take NSAIDs.73,74 Patients with cirrhosis and ascites75 and patients with significantly altered hemodynamic status can experience as much as a 50% decrease in creatinine clearance (ClCr) when treated with indomethacin (Indocin)76,77 or ibuprofen (Motrin). Some subjects with normal renal function experience profound changes in glomerular filtration rate when taking indomethacin concurrent with triamterene (Dyrenium).78
For E.T., who is fairly young and healthy without risk factors, the potential for NSAID-induced renal toxicity is quite low. Her renal function still should be monitored, however, if she is to be placed on an NSAID for more than a few days because she has recently undergone surgery and may have relative volume depletion.
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