Kee C S, Choi J W, Chang D K, Ahn Y H, Kim H J
Dept. of Internal Medicine, Hanyang University College of Medicine, Seoul, Korea.
J Korean Med Sci. 1993 Dec;8(6):464-70. doi: 10.3346/jkms.1993.8.6.464.
A 49-year-old man with liver cirrhosis and hypertension was found to have hyperkalemia out of a degree of renal insufficiency and metabolic acidosis with low to normal anion gap, aggravated by volume contraction with diarrhea and medications (captopril, spironolactone and atenolol) interfering with potassium homeostasis. Plasma renin activity and serum aldosterone levels of this patient on a regular diet after discontinuation of medications were very low compared to those of five other cirrhotic patients with normokalemia as controls. Also, the renin-aldosterone stimulation testing on this patient performed by sodium restricted diet and furosemide, upright position and by angiotensin converting enzyme inhibition (captopril, 50 mg) showed the blunted renin and aldosterone responses to each of these stimuli, almost no changes from baseline renin and aldosterone levels, it was concluded that the underlying defect responsible for hyperkalemia in this case was hyporeninemic hypoaldosteronism and this was aggravated by other factors or drugs affecting potassium homeostasis.
一名患有肝硬化和高血压的49岁男性,因肾功能不全和代谢性酸中毒(阴离子间隙低至正常)出现高钾血症,腹泻导致的容量收缩以及干扰钾稳态的药物(卡托普利、螺内酯和阿替洛尔)使其病情加重。与另外五名血钾正常的肝硬化患者作为对照相比,该患者停药后正常饮食时的血浆肾素活性和血清醛固酮水平非常低。此外,通过限制钠饮食和呋塞米、直立位以及血管紧张素转换酶抑制(卡托普利,50毫克)对该患者进行的肾素-醛固酮刺激试验显示,肾素和醛固酮对每种刺激的反应减弱,与肾素和醛固酮的基线水平几乎没有变化,得出结论,该病例中导致高钾血症的潜在缺陷是低肾素性低醛固酮血症,并且这被影响钾稳态的其他因素或药物加重。