Lee F O, Quismorio F P, Troum O M, Anderson P W, Do Y S, Hsueh W A
Department of Medicine, University of Southern California, LAC/USC Medical Center 90033.
Arch Intern Med. 1988 Feb;148(2):397-401.
We found that nearly 10% of 142 patients with systemic lupus erythematosus (SLE) had persistent, unexplained hyperkalemia. Renal mineralocorticoid resistance has been suggested to account for the hyperkalemia in SLE. We studied the renin-aldosterone response to intravenous furosemide (60 mg) and upright posture and the renin response to converting enzyme inhibition (captopril, 50 mg) and upright posture in five patients with SLE and hyperkalemia (group 1) and five normokalemic patients with SLE (group 2). Renal function was comparable. Plasma chloride level was higher and bicarbonate level slightly lower in group 1 than in group 2. Plasma cortisol level was normal in all patients. None of the patients was receiving nonsteroidal anti-inflammatory drugs or corticosteroids at the time of study. Basal plasma renin concentration and plasma aldosterone level were not significantly different between the two groups, although both tended to be higher in group 2. However, four of the five patients in group 1 had significantly blunted renin response to captopril compared with group 2. The same four patients also had blunted renin and aldosterone responses to furosemide. Thus, the majority of hyperkalemic patients with SLE had an impaired renin and aldosterone response to stimulation. We conclude that hyporeninemic hypoaldosteronism plays a key role in the pathogenesis of hyperkalemia in SLE.
我们发现，在142例系统性红斑狼疮（SLE）患者中，近10%存在持续的、原因不明的高钾血症。肾盐皮质激素抵抗被认为是SLE患者高钾血症的原因。我们研究了5例SLE合并高钾血症患者（第1组）和5例SLE血钾正常患者（第2组）对静脉注射速尿（60mg）和直立姿势的肾素-醛固酮反应，以及对转换酶抑制（卡托普利，50mg）和直立姿势的肾素反应。两组肾功能相当。第1组血浆氯水平高于第2组，碳酸氢盐水平略低于第2组。所有患者血浆皮质醇水平均正常。研究时所有患者均未服用非甾体抗炎药或皮质类固醇。两组基础血浆肾素浓度和血浆醛固酮水平无显著差异，尽管第2组两者均有升高趋势。然而，与第2组相比，第1组5例患者中有4例对卡托普利的肾素反应明显减弱。同样的4例患者对速尿的肾素和醛固酮反应也减弱。因此，大多数SLE合并高钾血症患者对刺激的肾素和醛固酮反应受损。我们得出结论，低肾素性低醛固酮血症在SLE患者高钾血症的发病机制中起关键作用。
