Persistent hypokalemia masking distal tubular acidosis and hypothyroidism: a case report

Abstract

Hypokalemic paralysis is an important reversible cause of acute flaccid weakness and may result from either intracellular potassium shift or true potassium depletion. Persistent hypokalemia associated with metabolic acidosis should be promptly evaluated for renal tubular disorders. We report a case of a 49-year-old man who presented with acute progressive quadriparesis and severe hypokalemia. Initial evaluation revealed serum potassium level of 1.5 mmol/l, metabolic acidosis, elevated creatine phosphokinase, renal potassium wasting, hypocalcemia with secondary hyperparathyroidism, and hypothyroidism. Despite potassium replacement, the patient demonstrated persistent hypokalemia ranging from 2.0-3.0 mmol/l and low serum bicarbonate levels across four months of outpatient follow-up. Urine studies and persistent acid-base abnormalities suggested an underlying distal renal tubular dysfunction. The patient improved clinically with potassium supplementation, supportive management with ongoing clinical monitoring during follow-up. This case highlights the importance of distinguishing hypokalemic paralysis secondary to chronic renal potassium wasting from isolated hypokalemic periodic paralysis.