Elsevier

The Lancet

Volume 316, Issue 8188, 2 August 1980, Pages 232-233
The Lancet

MEFENAMIC ACID NEPHROPATHY

https://doi.org/10.1016/S0140-6736(80)90122-1Get rights and content

Abstract

Non-oliguric renal failure developed in six elderly women who had been prescribed 1-2 g of mefenamic acid daily for 2-6 weeks for the relief of musculoskeletal pain.

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    Mefenamic acid (MFA), one of the nonsteroidal anti-inflammatory drugs (NSAIDs) that inhibits cyclooxygenase to suppress production of prostaglandin (Byron and Mark, 1998), is used for headaches, arthritis, and dysmenorrhea (Mcguak et al., 1996; Grillo et al., 2012). MFA sometimes causes liver (Robertson et al., 1980; Chan et al., 1991; Somchit et al., 2004), gastrointestinal, and kidney injuries (García and Jick, 1994; Davies, 1995), and some metabolites of MFA have been considered as causal factors for liver injury (Park et al., 2011; Vredenburg et al., 2014). MFA is converted to an acyl glucuronide (Gaganis et al., 2007), which may be related to liver injury, because of high reactivity (Sawamura et al., 2010).

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    One explanation for the obtained results might be a further reaction of initial hGST P1-1 adducts of 4′-OH-DF quinone imine with reactive oxygen species resulting from uncoupling by CYP102A1M11H, as was previously proposed to rationalize the oxygenation of troglitazone adducts [11]. Therapy with MFA is associated with cases of liver and renal injury that may result from formation of RMs and subsequent covalent modification of proteins [15,16,40]. MFA is metabolized in humans to reactive acylglucuronides [41], which were found to irreversibly modify human serum albumin and to bind to cellular proteins [42].

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    Within ten years of marketing, cases of non-oliguric renal failure were reported with mefenamic acid [10–13]. Histological examination provided evidence of renal papillary necrosis (RPN) in some individuals [10] while in others nephrotoxicity was consistent with allergic interstitial nephritis [11,13]. The latter is often characteristic of an immune mediated response to irreversible binding of either a drug or its metabolites to various cell proteins [14].

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