Besides the hereditary hyperkalaemic paralysis, a secondary form exists which often mimicks Guillain-Barre syndrome. A 62 year old patient is reported on who developed severe hyperkalaemic paralysis on the basis of mild renal failure and additive spironolactone intake. Neurophysiological examinations disclosed normal muscle fibre activity but delayed nerve conduction velocities indicating that the mechanism underlying secondary hyperkalaemic paralysis is different from channelopathies. Haemodialysis led to complete recovery. Review of the medical literature showed that spironolactone intake is the most common cause of secondary hyperkalaemic paralysis. Typical symptoms are flaccid tetraplegia sparing the cranial nerves with only mild or lacking sensory impairment. Symptoms promptly resolve after haemodialysis or after glucose and insulin infusion. Only three out of 18 patients reviewed died, because of cardiopulmonary complications. Thus the prognosis of secondary hyperkalaemic paralysis is good.