Irreversible Renal Failure following Mefenamic Acid

Dear Sir, Mefenamic acid has been implicated in a number of reports on acute reversible renal failure [1– 10]. Where renal biopsy has been undertaken, interstitial nephritis has been found in some cases [2, 4–7, 9, 10], and on cessation of the drug, an improvement in renal function has been observed. We report a case of irreversible acute renal failure due to interstitial nephritis progressing to interstitial fibrosis following the consumption of mefenamic acid. Case Report A 61-year-old male was admitted to hospital for treatment of a prolapsed intervertebral disc, L4/5. Treatment consisted of bed rest and skin traction, and analgesic treatment which included aspirin and mefenamic acid. Approximately 4 weeks later, he was transferred to this hospital for myelography. For 4 days prior to transfer, he had been unwell with diarrhoea and nausea, and had noted a diminution in his urine output. On arrival he was noted to be ill, slightly dehydrated and oliguric. Blood pressure was 120/80, and there was no evidence of a vasculitis. Serum biochemistry revealed a blood urea of 63.2 mmol/ 1, serum creatinine 1,573 μmol/l and urinalysis protein, but no casts. The serum creatinine 4 weeks previously had been within the normal range, and there was no history of analgesic abuse. Mefenamic acid treatment was withdrawn, and in view of his condition, he underwent emergency haemodialysis. A subsequent renal ultrasound examination revealed two normalsized kidneys; a renal biopsy was performed, which revealed a dense inflammatory cell infiltrate in the interstitium with fibrosis. There was superimposed tubulorrhectic tubular necrosis with an active tubulitis (fig. 1). The infiltrate involved both the cortex and the medulla, but was heavier in the medulla. The glomeruli displayed mesangial expansion and proliferation. In view of the biopsy findings, prednisolone (60 mg/day) was commenced. The patient remained oliguric and dialysis-dependent and 1 week later sustained an anterior myocar-dial infarction. Fig. 1. There is interstitial expansion with a brisk inflammatory infiltrate, early fibrosis and an active tubulitis. The glomerulus displays a mild degree of mesangial expansion and proliferation. HE ×170.