Mefenamic Acid Nephropathy
Author(s) -
M Segasothy,
A. Thyaparan,
A. N. Kamal,
Sri Sivalingam
Publication year - 1987
Publication title -
the nephron journals/nephron journals
Language(s) - English
Resource type - Journals
SCImago Journal Rank - 0.951
H-Index - 72
eISSN - 2235-3186
pISSN - 1660-8151
DOI - 10.1159/000184100
Subject(s) - medicine , mefenamic acid , nephropathy , kidney disease , nephrology , pharmacology , endocrinology , diabetes mellitus
Dr. M. Segasothy, Department of Medicine, Royal Melbourne Hospital, Parkville, Melbourne, Victoria, 3052 (Australia) Dear Sir, Analgesic nephropathy has most commonly been attributed to the excessive consumption of analgesic compounds commonly containing aspirin, phenacetin and caffeine. Occasional examples of renal papillary necrosis (RPN) with individual analgesics such as aspirin, indomethacin or phenylbutazone have been described but these are uncommon because individual analgesics are rarely addictive [1]. Mefenamic acid has been reported to cause reversible nonoliguric renal failure [2–6], interstitial nephritis [4–6] and oliguric renal failure associated with glomerulo-nephritis and widespread vasculitis [7]. We report two cases of RPN due to the consumption of mefenamic acid. Case Reports Case 1 is a 47-year-old male factory worker who had been consuming mefenamic acid (500 mg) regularly for his gouty arthritis since 1975. His consumption of mefenamic acid had been 3 capsules daily from 1975 to 1977,10 capsules monthly from 1978 to 1984 and 3 capsules monthly over the past year. All in all, he had had consumed about 4,200 capsules of mefenamic acid. He denied the consumption of other analgesics. In 1977 he developed hypertension and was also operated on for left renal calculus. He presented in May 1985 with hematuria. He had no past history of diabetes or tuberculosis. Investigations showed hemoglobin 12.5 g/dl, urea 7.8 mmol/l creat-inine 200 μmol/l and uric acid 580 μmol/l. Urinalysis showed 2 + protein, 5 · 106 leukocytes and 20 · 106 red cells per liter, no epithelial cells or casts and no organisms on culture. However, repeat urinalysis 2 weeks later revealed no abnormalities. The urine ferric chloride test for aspirin was negative. Intravenous urogram (IVU) showed bilateral papillary necrosis. Case 2 is a 58-year-old female who presented in December 1984 for recurrent episodes of hematuria of 1 month duration. She has been hypertensive for more than 10 years. She has osteoarthritis of both knees for which she had been consuming about 10 capsules of mefenamic acid (500 mg) weekly for the past 2 years, giving a total of about 1,000 capsules. She denied the consumption of other analgesics. She has had no past history of diabetes or tuberculosis. Investigations showed hemoglobin 12.9 g/dl, urea 7.4. mmol/l, creatinine 120 μmol/l and uric acid 424 μmol/l. Urinalysis showed trace of protein, red cells 200 · 10V1, no leukocytes, epithelial cells or casts and no organisms on culture. The urine ferric chloride test for aspirin was negative. IVU showed bilateral papillary necrosis.
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