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Dr. Noritomo Itami, Hokkaido University School of Medicine, Department of Pediatrics, North 15 West 7, Kita-ku, Sapporo 060 (Japan) Dear Sir, We read the paper by Boletis et al. [1] with interest, we would like to add a similar case and suspect that mefenamic acid may promote the progression to interstitial fibrosis in some cases. A 13-year-old boy was given mefenamic acid (500 mg/day for 1 week and then 750 mg/day) in addition to coumarin in order to control proteinuria (3 g/day) and hypoproteinuria (below 5 g/l). At the age of 5, he was found to have proteinuria. At the age of 8, treatment with dipyridamole and indomethacin was started at another hospital. Proteinuria still continued and he was referred to us. At the age of 11, a renal biopsy was performed and focal segmental glomerulosclerosis was suspected. The above treatment was withdrawn and treatment with glucocorticoid and heparin which followed coumarin and dipyridamole was tried but no response was observed. Before the treatment with mefenamic acid, serum biochemistry revealed a blood urea level of 8.5 mmol/l, serum creatinine 71 mol/l, serum total protein 4.8 g/l, and 3+ proteinuria without hematuria. During the treatment, urine volume did not decrease compared with that before the treatment and there were no rash or complaints except gastrointestinal upsets which included loose stools, vomiting, and anorexia and resolved spontaneously. Eight months later, an increase in serum creatinine (132 mol/l) was noticed and mefenamic acid was stopped. However, renal failure progressed gradually (fig. 1). The nephrotoxicity of mefenamic acid is well known [2,4], and the clinical picture is usually one of nonoliguric renal failure, which is reversed when mefenamic acid is stopped as renal failure due to NSAIDs is generally reversible [5]. Most studies show that NSAID-induced renal failure is due to the diminished renal vasodilatory effect of prostaglandins [5]. However, the machanism of toxicity in our case seems to be unrelated to inhibition of prostaglandin synthesis since our patient had normal renal function while continuing to take indomethacin, which is a more potent prostaglandin synthetase inhibitor than mefenamic acid. PSLl ADτ|30rτ3⁄8 J mefenamic acid 750 mg 1 ×