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Letters to the Editor| Volume 57, ISSUE 4, P575, October 2019

Response to Letter to the Editor

      Thank you for the interesting comments by Dr. Jolobe in this issue of the Journal (

      Jolobe OM. Mineralocorticoids as a treatment for selected cases of refractory hyperkalemia. J Emerg Med.

      ). Although his review of the use of mineralocorticoid treatment of hyperkalemia has a plausible mechanism of action, the limitation to refractory hyperkalemia excludes this strategy for the overwhelming majority of emergency department (ED) cases. Our study investigated the initial ED treatment of hyperkalemia, and had a primary endpoint defined as the serum potassium level after 4 h of treatment (
      • Peacock W.F.
      • Rafique Z.
      • Clark C.L.
      • et al.
      Real world evidence for treatment of hyperkalemia in the emergency department (REVEAL-ED).
      ). Because the definition of refractory hyperkalemia requires a failure of standard therapy, it is outside the purview of our study to provide insight regarding treatment with mineralocorticoids. Further, we are not aware of a single prospective study using mineralocorticoid therapy for the ED treatment of hyperkalemia. We cannot support the use of mineralocorticoid therapy as an appropriate intervention until there are prospective safety and efficacy data in the ED environment.
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      References

      1. Jolobe OM. Mineralocorticoids as a treatment for selected cases of refractory hyperkalemia. J Emerg Med.

        • Peacock W.F.
        • Rafique Z.
        • Clark C.L.
        • et al.
        Real world evidence for treatment of hyperkalemia in the emergency department (REVEAL-ED).
        J Emerg Med. 2018; 55: 741-750

      Linked Article

      • Mineralocorticoids as a Treatment for Selected Cases of Refractory Hyperkalemia
        Journal of Emergency MedicineVol. 57Issue 4
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          Peacock et al. documented diabetes as a possible cause of hyperkalemia in 27% of the 203 subjects in the multicenter prospective observational study of hyperkalemia (1). This observation has important implications, given the fact that diabetic nephropathy is a risk factor for type 4 renal tubular acidosis, and associated hyporeninemic hypoaldosteronism, which may be unmasked by drugs such as trimethoprim, leading to severe hyperkalemia (2,3). In the report by Hussain and Chowdhury (2016) (3), of a 75-year-old woman with type 2 diabetes currently on trimethoprim, the administration of glucose/insulin infusion and intravenous sodium bicarbonate could only bring down her admission serum potassium level of 8.8 mEq/L to levels in the range 6.0 to 7.0 mEq/L.
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