MEFENAMIC ACID NEPHROPATHY
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Cited by (68)
Human superoxide dismutase 1 attenuates quinoneimine metabolite formation from mefenamic acid
2021, ToxicologyCitation Excerpt :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).
Mini-dialysis tubes as tools to prepare drug-protein adducts of P450-dependent reactive drug metabolites
2015, Journal of Pharmaceutical and Biomedical AnalysisCitation Excerpt :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].
Renal Organic Cation and Anion Transport: From Physiology to Genes
2010, Comprehensive Toxicology, Second EditionGlucuronidation of fenamates: Kinetic studies using human kidney cortical microsomes and recombinant UDP-glucuronosyltransferase (UGT) 1A9 and 2B7
2007, Biochemical PharmacologyCitation Excerpt :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].
Organic anion transporter (Slc22a) family members as mediators of toxicity
2005, Toxicology and Applied PharmacologyNephrotoxicity of nonsteroidal anti-inflammatory drugs: Physiologic foundations and clinical implications
1999, American Journal of Medicine