Medizinische Klinik und Poliklinik IV, Klinikum der Universität München, Ziemssenstr. 1, 80336 München, Germany.
J Clin Endocrinol Metab. 2012 Nov;97(11):3965-73. doi: 10.1210/jc.2012-2234. Epub 2012 Aug 14.
Unilateral adrenalectomy is the therapy of choice in aldosterone-producing adenoma (APA). Zona glomerulosa (ZG) insufficiency causing hyperkalemia after adrenalectomy has been described in case reports.
Our aim was to analyze the clinical relevance of ZG insufficiency causing hyperkalemia after adrenalectomy in a large series of patients with APA.
This was a retrospective chart review.
The study was conducted at two tertiary university referral centers in Germany.
Data from 110 patients with confirmed APA adrenalectomized at the centers in Munich and Berlin between 2004 and 2012 were analyzed.
The primary outcome was the incidence of ZG insufficiency causing hyperkalemia after adrenalectomy; the secondary outcome was the identification of risk factors predisposing for hyperkalemia.
Eighteen of 110 patients (16%) developed postoperative hyperkalemia. The majority of these patients (n = 14) had undetectable plasma aldosterone levels after adrenalectomy; four had low aldosterone levels. In 12 of these patients, hyperkalemia was documented only once and resumed spontaneously. Prolonged hypoaldosteronism accompanied by hyperkalemia was observed in six patients (5% of total cohort). These patients needed continuous mineralocorticoid replacement therapy for 11-46 months. Mineralocorticoid antagonist treatment for 4 wk prior to surgery did not prevent hyperkalemia. In multivariate analysis, preoperatively decreased glomerular filtration rate and increased serum creatinine as well as increased postoperative creatinine and microalbuminuria remained significant predictors of hyperkalemia.
Persistent postoperative hypoaldosteronism with hyperkalemia occurs in 5% of adrenalectomized PA patients through prolonged ZG insufficiency, requiring long-term fludrocortisone treatment. Potassium levels after adrenalectomy must be monitored to avoid life-threatening hyperkalemia.
在醛固酮瘤（APA）中，单侧肾上腺切除术是治疗的首选方法。已有个案报道称，肾上腺切除术后由于球状带（ZG）功能不全导致高钾血症。
我们旨在分析大量 APA 患者中由于肾上腺切除术后 ZG 功能不全导致高钾血症的临床相关性。
这是一项回顾性图表分析。
该研究在德国的两个三级大学转诊中心进行。
分析了 2004 年至 2012 年期间在慕尼黑和柏林中心接受确诊的 APA 肾上腺切除术的 110 名患者的数据。
主要结局是肾上腺切除术后由于 ZG 功能不全导致高钾血症的发生率；次要结局是确定导致高钾血症的易患因素。
110 例患者中有 18 例（16%）术后发生高钾血症。这些患者中大多数（n=14）术后血浆醛固酮水平无法检测到；4 例患者的醛固酮水平较低。其中 12 例患者仅记录到一次高钾血症，且自行恢复。6 例患者（占总队列的 5%）观察到持续的低醛固酮血症伴高钾血症。这些患者需要连续接受 11-46 个月的盐皮质激素替代治疗。术前 4 周使用盐皮质激素拮抗剂治疗并未预防高钾血症。多变量分析显示，术前肾小球滤过率和血清肌酐降低以及术后肌酐和微量白蛋白尿增加仍然是高钾血症的显著预测因素。
通过延长 ZG 功能不全，持续术后低醛固酮血症伴高钾血症在 5%的肾上腺切除术 PA 患者中发生，需要长期接受氟氢可的松治疗。必须监测肾上腺切除术后的血钾水平，以避免危及生命的高钾血症。
