Hyponatremia Associated with Prophylactic Low-Dose Trimethoprim during Systemic Corticosteroid Therapy for AQP4-Positive Optic Neuritis in a Diabetic Patient.
Masahiro TakuboSho TanakaMasaru KushimotoJin IkedaKatsuhiko OgawaYutaka SuzukiMasanori AbeHisamitsu IshiharaMidori FujishiroPublished in: Antibiotics (Basel, Switzerland) (2020)
Hyponatremia associated with low-dose trimethoprim in patients on concomitant systemic corticosteroid therapy has rarely been reported. Here, we describe a 57-year-old woman with a history of diabetes mellitus and hypertension treated with telmisartan, who presented with progressive visual impairment of the left eye due to anti-aquaporin-4 antibody-positive optic neuritis. The patient received pulsed intravenous methylprednisolone followed by oral prednisolone at 30 mg/day and trimethoprim-sulfamethoxazole prophylaxis (160 mg and 800 mg daily). Her serum sodium level steadily decreased, and the potassium level was slightly elevated despite well-preserved renal function. This state persisted even after telmisartan discontinuation. In addition to hypotonic hyponatremia (125 mEq/L) with natriuresis, hyperkalemic renal tubular acidosis was diagnosed based on normal anion gap metabolic acidosis and hyperkalemia with low urinary potassium excretion. After trimethoprim-sulfamethoxazole cessation, electrolytes and acid-base imbalances swiftly recovered. We can conclude that caution must be exercised when treating such patients, because even low-dose trimethoprim may cause hyponatremia concomitant with hyperkalemic renal tubular acidosis, despite the mineralocorticoid effects of systemic corticosteroids.
Keyphrases
- low dose
- high dose
- end stage renal disease
- newly diagnosed
- ejection fraction
- chronic kidney disease
- prognostic factors
- blood pressure
- stem cells
- heart failure
- optical coherence tomography
- acute heart failure
- atrial fibrillation
- ionic liquid
- microbial community
- skeletal muscle
- insulin resistance
- endothelial cells
- wastewater treatment
- antibiotic resistance genes
- smoking cessation
- high glucose