Mineralocorticoids as a Treatment for Selected Cases of Refractory Hyperkalemia

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 ( ). 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 ( , ). In the report by Hussain and Chowdhury (2016) ( ), 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. Nevertheless, within 48 h of administration of fludrocortisone 100 μg bid by mouth, plasma potassium was restored to the normal range ( ). Further investigations revealed a serum creatinine level of 191 μmol/L (2.16 mg/dL), and a random serum cortisol of 423 nmol/L (15.3 μg/dL) ( ). Tacrolimus is another inducer of Type 4 renal tubular acidosis (RTA), and the resulting hyperkalemia may be refractory to intravenous furosemide, oral sodium polystyrene, intravenous sodium carbonate, and glucose-insulin infusion ( ). In the report by Sahu et al. (2017) ( ), however, serum potassium fell from 6.2 mmol/L (6.2 mEq/L) to the normal range 24 h after the administration of fludrocortisone 0.1 mg/day. With continued use of fludrocortisone, the serum potassium subsequently fell to 4.5 mmol/L (4.5 mEq/L) ( ).