Radó J P
Department of Medicine, Emil Weil Hospital, Budapest, Hungary.
Int J Clin Pharmacol Ther Toxicol. 1988 Jul;26(7):339-45.
Hyperkalemic 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.
一名76岁患有慢性肾功能不全的女性在使用螺内酯进行抗高血压治疗期间出现了高钾性弛缓性四肢瘫痪和心脏毒性紊乱。高钾血症得到成功纠正，随后所有心脏和肌肉紊乱症状均消失。在三年的观察期内，肾脏疾病进展导致肌酐清除率从85 ml/分钟降至4.5 ml/分钟，这本身显然对血清钾水平没有影响。我们的研究表明，肾素-醛固酮和糖皮质激素系统的原发性功能不全并非高钾血症的原因，因此，高钾血症完全可能是由于螺内酯消除了已经减少的肾单位的钾分泌能力所致。进一步研究表明，除了钾潴留外，该药物对氢离子分泌的阻断作用（“肾小管酸中毒”）在螺内酯诱导的高钾血症发生过程中可能也起到了作用。
