Cotrimoxazole
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Acute interstitial nephritis and nephrogenic diabetes insipidus: case report A 53-year-old man developed acute interstitial nephritis and nephrogenic diabetes insipidus during treatment with cotrimoxazole for Pneumocystis jiroveci pneumonia prophylaxis [time to reactions onsets not stated]. The man presented with a 4-day history of nocturia, polydipsia and polyuria (current presentation). His physical examination was notable for dehydration. Six months before the presentation, he was diagnosed with right temporal lobe glioblastoma multiforme, and had undergone temporal lobe resection 3 months previously. He also completed a 6 week course of adjuvant chemotherapy with temozolomide and radiotherapy. He had been receiving cotrimoxazole [sulfamethoxazole-trimethoprim] sulfamethoxazole 800mg/trimethoprim 160mg three times a week as prophylaxis of Pneumocystis jiroveci pneumonia. At admission (at the current presentation), his serum creatinine and urea levels indicated acute kidney injury. Additionally, his serum sodium, serum osmolality and plasma copeptin levels were high, while remaining test results were normal. His haemoglobin A1c and plasma glucose levels were normal, which ruled out the possibility of diabetes mellitus. His urinary investigations showed leucocyturia and mild microalbuminuria. An ultrasound of the urinary tract revealed normal kidneys, while brain MRI revealed oedema at the surgical site. Two weeks previously (following completion of temozolomide and radiotherapy), his serum sodium and serum creatinine levels were noted as 142 mmol/L and 85 µmol/L, respectively. His treatment with cotrimoxazole was continued until the current presentation. Based on his presentation and high levels of copeptin, a diagnosis of nephrogenic diabetes insipidus caused by acute kidney injury was made. Therefore, the man received IV rehydration therapy for dehydration. After fluid resuscitation, he stayed polyuric. Subsequently, he started receiving treatment with hydrochlorothiazide for nephrogenic diabetes insipidus. However, further deterioration of kidney function was noted. Hence, a kidney biopsy was performed, and subsequent histological examination showed 20 glomeruli, of which, two glomeruli were globally sclerosed. Also, active focal tubulointerstitial change including tubular dilatation, regenerative and degenerative epithelial change and chronic interstitial inflammation wit isolated oeosinophils were observed. Immunofluorescent investigation and electron microscopy showed normal results. Therefore, a diagnosis of cotrimoxazole-induced acute interstitial nephritis was made. Treatment with cotrimoxazole was stopped, and hydrochlorothiazide was up-titrated. Subsequently, polydipsia and polyuria resolved, and his kidney function improved. One month after the presentation, he was re-started on temozolomide. During temozolomide therapy, his kidney function stayed stable. His proteinuria resolved, and urinary sodium and urinary albumin creatinine ratio remained unchanged. Athavale A, et al. Acute interstitial nep
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