Division of Internal Medicine and Hypertension Unit Division of Cardiology, Department of Medical Sciences, University of Torino, Torino Division of Internal Medicine, Department of Medicine, University of Udine, Udine, Italy Division of Clinical Hypertension, Endocrinology and Metabolism, Tohoku University Graduate School of Medicine, Sendai, Japan.
J Hypertens. 2020 Jan;38(1):3-12. doi: 10.1097/HJH.0000000000002216.
In experimental animal models, exogenous aldosterone excess has been linked to the progression of renal disease. However, the evidence of an increased risk of renal damage in patients affected by primary aldosteronism remains controversial. We aimed at evaluating the association between primary aldosteronism and renal damage through a meta-analysis.
We performed a quantitative review of studies evaluating parameters of renal function in patients affected by primary aldosteronism compared with hypertensive patients without primary aldosteronism and in patients affected by primary aldosteronism before and after treatment. We searched MEDLINE, EMBASE, and the Cochrane Central Register of Controlled Trials from January 1960 up to April 2019.
Forty-six studies including 6056 patients with primary aldosteronism and 9733 patients affected by arterial hypertension without primary aldosteronism were included. After 8.5 years from hypertension diagnosis, patients with primary aldosteronism had an increased estimated glomerular filtration rate (eGFR) compared with hypertensive patients without primary aldosteronism [by 3.37 ml/min IQR (0.82-5.93)] and a more severe albuminuria [standard mean difference 0.55 (0.19-0.91)], resulting into an association with microalbuminuria [odds ratio (OR) 2.09 (1.40; 3.12)] and proteinuria [OR 2.68 (1.89;3.79)]. Following primary aldosteronism treatment, after a median follow-up of 12 months, a reduction in eGFR was observed [by -10.69 ml/min (-13.23; -8.16)], consistent in both medically and surgically treated patients. Similarly, a reduction in albumin excretion and an increase in serum creatinine were observed after treatment.
Patients affected by primary aldosteronism, compared with patients affected by arterial hypertension without primary aldosteronism, display a more pronounced target organ damage, which can be mitigated by the specific treatment.
在实验动物模型中,外源性醛固酮过多与肾脏疾病的进展有关。然而,原发性醛固酮增多症患者发生肾损伤风险增加的证据仍存在争议。我们旨在通过荟萃分析评估原发性醛固酮增多症与肾损伤之间的关系。
我们对评估原发性醛固酮增多症患者与无原发性醛固酮增多症的高血压患者以及原发性醛固酮增多症患者治疗前后肾功能参数的研究进行了定量综述。我们检索了 1960 年 1 月至 2019 年 4 月期间的 MEDLINE、EMBASE 和 Cochrane 对照试验中心注册库。
共纳入 46 项研究,包括 6056 例原发性醛固酮增多症患者和 9733 例无原发性醛固酮增多症的高血压患者。原发性醛固酮增多症患者从高血压诊断后 8.5 年开始,其估算肾小球滤过率(eGFR)高于无原发性醛固酮增多症的高血压患者[增加 3.37ml/min IQR(0.82-5.93)],且白蛋白尿更严重[标准均数差 0.55(0.19-0.91)],因此与微量白蛋白尿[比值比(OR)2.09(1.40;3.12)]和蛋白尿[OR 2.68(1.89;3.79)]相关。在原发性醛固酮增多症治疗后,中位随访 12 个月时,观察到 eGFR 下降[下降 10.69ml/min(-13.23;-8.16)],在药物和手术治疗的患者中均观察到这种下降。同样,治疗后白蛋白排泄减少和血清肌酐增加。
与无原发性醛固酮增多症的高血压患者相比,原发性醛固酮增多症患者的靶器官损伤更为明显,这种损伤可以通过特异性治疗得到缓解。