INTRODUCTION:
Hyperkalemia is defined as an increase in the serum potassium levels
above the upper limit of normal, which is higher than 5-5.5 mEq/L. The
patients with hyperkalemia present as asymptomatic in the mildly
elevated serum levels to muscle weakness, periodic paralysis,
life-threatening cardiac arrhythmias in higher serum potassium levels.
Usually, the symptoms of hyperkalemia develop when the serum potassium
levels are higher than 6-7 mEq/L. Hyperkalemia can occur due to various
causes like increased intake, altered intracellular shifts
(hyperglycemia, metabolic acidosis), increased tissue catabolism
(trauma, burns, tumor lysis syndrome), and impaired excretion in acute
or chronic renal failure. Drug-induced hyperkalemia is also occasionally
encountered in clinical practice. In a study by
Elena
Ramírez et al, the incidence of life-threatening drug-induced
hyperkalemia was reported as 3 per 10,000 admissions.1 Common causes of drug-induced hyperkalemia are
Angiotensin-converting enzyme inhibitors, Angiotensin receptor blockers,
Potassium-sparing diuretics, cardiac glycosides, Nonselective
beta-blockers, cyclosporine, etc. Trimethoprim-sulfamethoxazole
(Cotrimoxazole) is one such drug causing hyperkalemia, which is used as
a prophylaxis of choice for Pneumocystis jiroveci in patients with solid
organ transplant. We present a case of TMP-SMX induced hyperkalemia in a
renal transplant patient.