Nimesulide and acute renal failure caused by oxalate precipitation.

Sir, Acute renal failure (ARF) seen with non-steroidal anti-inflammatory drugs (NSAIDs) is mainly haemodynami-cally mediated due to inhibition of the synthesis of renal prostaglandins (PGs) w1x. Nimesulide is a new generation NSAID that differs from conventional NSAIDs in structure and pharmacological profile, claiming fewer side effects due to the specificity for the COX-2 enzyme w2x. We describe a patient presenting ARF following intake of several tablets of nimesulide. Case. A 40-year-old man was admitted with right-sided loin pain, asthenia, and gastrointestinal complaints of 1 week. One month before admission he had a torsio of the right ankle for which nimesulide was prescribed in a dose of two tablets of 200 mguday. In total, the patient had taken 28 tablets or 5600 mg nimesulide. No other medication or vitamins have been taken. Medical history revealed the presence of microscopic haematuria since the age of 20, discovered on routine medical examination during duty. However, a clinical investigation was never performed. There was no history of familial nephropathy. Physical examination showed a well-fed, well-hydrated, ill-looking man. The patient was normotensive, had no fever nor adenopathies or rash. Ankle oedema was absent, but fluid retention was suspected as the patient reported a weight gain of 7 kg during the last two weeks. Initial laboratory tests showed ARF (s-creatinine 10.86 mgudl (normal levels 0.5–1.5 mgudl), urea 142 mgudl (normal levels 15– 40 mgudl), normal potassium). Fibrinogen was 488 mgudl (normal levels 180– 400 mgudl), C-reactive protein 21 mgul (normal level up to 4 mgul) and elevated sedimentation rate 35 mmuh (normal levels 0–10 mmuh). White blood cell (WBC) count and total number of eos-inophils were within the normal range. Urine analysis disclosed rare WBC, numerous RBC, no casts. Urine culture was negative. Creatinine clearance was 6 mlumin. The test for urinary myoglobin was negative. Proteinuria was 0.82 guday and glucosuria was absent. Hyperuricaemia of 16 mgudl was noted (normal levels 3.4 –7.0 mgudl), but with low urinary uric acid concentration: 71 mgu24 h (normal levels 250–750 mgu24 h). The urinary uric acid to creatinine ratio was less than 1 (FEUA s 0.48). Bacterial and viral infection was excluded by appropriate testing. Complement study and serum-IgA were in the normal range and nuclear antibodies and ANCA were negative. Despite severe renal failure oxaluria was still 18 mguday. In subjects with normal renal function and on a normal diet, oxalate excretion ranges from 10 to 45 mguday. …