Severe Hypokalemia After Corticosteroid Use: A Case of Steroid-Induced Potassium Depletion

Hypokalemia can cause muscle weakness and life-threatening arrhythmias. Glucocorticoids can lower potassium through mineralocorticoid receptor activity and enhanced distal sodium reabsorption, and extensive topical corticosteroid use can also contribute. Clinicians must be able to identify the source of potassium loss and correct the deficit quickly. Here, we present a 35-year-old man with hypertension, obesity, and obstructive sleep apnea who developed five days of weakness soon after starting a prednisone 50 mg taper and triamcinolone 0.1% cream. Serum potassium was 1.9 mmol/L with creatinine 0.94 mg/dL. Spot urine analysis showed an osmolality of 551 mOsm/kg, potassium of 5 mmol/L, creatinine of 121 mg/dL, and chloride of 60 mEq/L. The urine potassium-to-creatinine ratio was 4.1 mEq/g, which is below the threshold that indicates renal potassium wasting in hypokalemia. The transtubular potassium gradient was 1. There was no ECG abnormality. He received 320 mEq of potassium with improvement to 5.1 mmol/L. After stopping steroids and acyclovir, potassium normalized with no sequela after six weeks. Severe hypokalemia can be multifactorial in new steroid users. In this patient, a significant total body potassium deficit, accompanied by a low transtubular potassium gradient, suggested non-renal losses with superimposed steroid exposure and other contributing factors. This case is notable for severe hypokalemia with low urinary potassium indices shortly after starting oral prednisone and large‑area topical triamcinolone, with normalization after withdrawal and repletion. When initiating systemic or high surface area topical corticosteroids, clinicians should monitor for side effects, including hypokalemia, review concurrent agents that affect tubular function, and use urine indices to localize losses. Early recognition of potential triggers can prevent arrhythmia and reduce complications.