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.