Naproxen
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Acute interstitial nephritis and renal cortical necrosis: case report A 62-year-old man developed acute interstitial nephritis and renal cortical necrosis during treatment with naproxen for migraine. The man presented with nausea, fever, vomiting and bilateral flank pain for 2 days. He exhibited breathlessness and bilateral pedal oedema. Of note, he had been receiving oral naproxen 500mg twice daily for migraine for 1 week before admission, alongside losartan for management of his BP. On examination, he appeared febrile and exhibited tachypnoea, with a BP of 170/90mm Hg. Bilateral basal coarse crepitations were heard on chest auscultation. Bilateral pedal oedema was noted. Laboratory investigations revealed metabolic acidosis. Other notable analyses were: serum creatinine 3.1 mg/dL, serum sodium 127 meq/L, serum potassium 5.4 meq/L, random blood sugar 200 mg/dL and haemoglobin 10.1 g/dL. Total WBC count was 19800/cu.mm with neutrophils 75%, lymphocytes 2.9%, eosinophils 14.5%. His platelet count was 1.8L/cu.mm. He had eosinophilic leukocytosis and eosinophiluria. An ultrasonogram of his abdomen revealed mildly enlarged kidneys; both kidneys were hyperechoeic in echotexture with normal pelvicalyceal system. CT scan of abdomen revealed mildly enlarged kidneys and normal collecting system. Based on these findings, a provisional diagnosis of acute pyelonephritis was made. The man started receiving unspecified broad-spectrum parenteral antibiotics. However, no urinary tract symptoms were observed, and an abdomen ultrasonogram ruled out the possibility of obstructive uropathy or any collection or abscess. Urine microscopy revealed 3+ albumin, RBC 1/hpf and WBC 24/hpf. Peripheral blood smear was negative for haemoparasites, atypical cells and schistocytes. Further analyses ruled out infectious aetiologies. The possibilities of Raynaud’s phenomenon, livedo reticularis, rash or Hollerhorst plaque were also ruled out. He did not have a history of use of poisonous substances and had not ingested any medications lately, apart from losartan and naproxen. Also, he neither had a history of insect or snake bite, nor recent severe physical exertion. Acute pancreatitis was ruled out due to lack of evidence. Further worsening of renal failure was noted, and he became oligoanuric with symptoms of severe uremia and worsening breathlessness. He was placed on haemodialysis via non‑tunneled internal jugular venous catheter. Persistent fever spikes were noted in spite of unspecified broad-spectrum antibiotics; however, his urine and blood cultures remained sterile, without evidence of sepsis. Serial blood counts revealed a progressive increase in eosinophils. Given the background of eosinophilia, he was suspected to have drug-induced fever; hence, antibiotic therapy was discontinued. There was no improvement in renal function over a period of 10 days. Renal biopsy showed patchy cortical necrosis and dense eosinophilic infiltrate admixed with lymphoplasmacytic inflammatory infiltrates and focal interstitial oedema, which indicate
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