Octreotide‐ or Trimethoprim‐Induced Hyperkalemia?

The article by Sargent et al 1 associating hyperkalemia with octreotide in a 68‐year‐old, 91‐kg trauma victim has little focus on other potential causes of her hyperkalemia. Her medical history was significant for noninsulin‐dependent diabetes mellitus. The authors, however, do not state how long she had this disease and whether she had any evidence of end‐organ damage. The episode of postoperative hypotension, as well as the assumed oliguria (her serum creatinine increased from 1.5 to 2.3 mg/dl) on day 3 of hospitalization, clearly contributed to renal hypoperfusion and potential renal injury. There was no other mention of renal impairment until the laboratory values revealed a serum creatinine of 2.5 mg/dl and a blood urea nitrogen of 91 mg/dl on day 14 of hospitalization. The patient appeared to be volume depleted (blood urea nitrogen:serum creatinine ratio > 20:1, serum sodium 154 mmol/L), and her potassium may have been lower (4.1 mmol/L) secondary to the effects of aldosterone. Interestingly, on day 11, oral (suspension?) trimethoprim‐sulfamethoxazole (TMP‐SMX) 180 mg twice/day (4 mg/kg/day TMP) was started for a urinary tract infection. The next day (day 12), this was changed to the intravenous route at a dose of 320 mg every 8 hours (∼11 mg/kg/day TMP) for suspected pneumonia. The patient's serum potassium was already beginning to rise slowly (4.1 to 4.6 mmol/L) even before the start of octreotide on day 16 despite improving serum creatinine (2.5 to 1.2 mg/dl) and serum sodium (154 to 147 mmol/L).