Cotrimoxazole
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Salt losing nephropathy and hyponatraemia: case report A 72-year-old man developed salt-losing nephropathy (SLN) and hyponatraemia during treatment with cotrimoxazole for pulmonary nocardiosis. The man, who was hospitalised due to with community-acquired pneumonia and acute exacerbation of COPD, treated with piperacillin/tazobactam, levofloxacin and prednisone. Subsequently, he was found to have pulmonary nocardiosis, and he started receiving double-strength cotrimoxazole [trimethoprim/sulfamethoxazole, Bactrim; route not stated] 160/800mg, three tablets twice daily. He received 10 mg/kg/day of trimethoprim in two divided doses (recommended dose 5–10 mg/kg/day for pulmonary nocardiosis in immunocompetent patients). He was then discharged. His other significant discharge medications included citalopram, allopurinol and prednisone. However, 5 days post discharge, he presented with confusion. His laboratory investigation showed low levels of sodium, chloride, uric acid and serum osmolality. His urine sodium was found to be 109 mmol/L. Based on the findings, he was initially diagnosed as syndrome of inappropriate antidiuretic hormone secretion (SIADH) secondary to citalopram. He was then admitted to the ICU. The man’s therapy with citalopram was stopped, and a strict fluid restriction of 800 mL/24 hours was initiated. However, his serum sodium level dropped to 108 mmol/L within the next 18 hours. He experienced worsening of confusion, and hypertonic sodium-chloride [saline] was initiated. His serum sodium improved to 114 mmol/L, with an improvement of the mental status, but on withdrawal of the hypertonic sodium-chloride, the sodium level again reduced to 110 mmol/L. Repeat urine sodium and osmolality were persistently high. He was then treated with salt tablets, and his serum sodium stayed between 112–114 mmol/L for the following 48 hours. At this point, the diagnosis of SIADH was considered as differential, and a diagnosis of SLN secondary to trimethoprim was considered. In order to confirm the diagnosis of SLN, a bedside ultrasound examination of the inferior vena cava (IVC) was performed to assess right atrial pressure and overall volume status. The IVC measured 0.7cm proximal to the hepatic vein with complete inspiratory collapse, which was consistent with intravascular subclinical volume depletion. Thus, a diagnosis of SLN was confirmed. Therapy with cotrimoxazole was then discontinued, and he was treated with normal sodium-chloride. His sodium level improved gradually, and following 4 days, his serum sodium was found to be 124 mmol/L. Thereafter, he was discharged back to the nursing home with salt tablets. His sodium level normalised in about 2 weeks after the hospital discharge. Saha BK, et al. Trimethoprim-induced hyponatremia mimicking SIADH in a patient with pulmonary nocardiosis: use of point-of-care ultrasound in apparent euvolemic 803502516 hypotonic hyponatremia. BMJ Case Reports 13: no pagination, No. 8, 25 Aug 2020. Available from: URL: http://doi.org/10.1136/bcr-2020-235558
0114-9954/20/1823-00
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