• J P Radó.
• Department of Medicine, Emil Weil Hospital, Budapest, Hungary.
• Int J Clin Pharmacol Ther Toxicol. 1988 Jul 1; 26 (7): 339-45.

AbstractHyperkalemic flaccid quadriplegia and cardiotoxic disturbances developed during antihypertensive therapy with spironolactone in a 76-year-old woman with chronic renal insufficiency. Hyperkalemia was successfully overcome and followed by the disappearance of all cardiac and muscular disorders. Progression of the renal disease leading to a decrease of creatinine clearance from 85 ml/min to 4.5 ml/min, during a three-year observation period per se had apparently no influence on the serum level of potassium. Our studies suggested that no primary insufficiency of the renin-aldosterone and glucocorticoid systems had been responsible for the hyperkalemia, therefore, it could be contributed entirely to the effect of spironolactone abolishing the K+ secreting capacity of the already decreased renal mass. Further studies revealed that blocking action of the drug on H+ secretion ("renal tubular acidosis") may also have had a role-in addition to the K+ retention-in the development of the spironolactone-induced hyperkalemia.

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