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局灶性肾纤维肌发育不良中的高肾素型高血压:经肾血管成形术阻断肾素系统血管紧张素过度激活治愈了高血压并迅速逆转了心肌肥厚。

High renin hypertension in focal renal fibromuscular dysplasia: turn off of renin system angiotensin overactivation by renal angioplasty cured high blood pressure and quickly reversed myocardial hypertrophy.

机构信息

Centro per lo Studio dell'Ipertensione Arteriosa e delle malattie Cardiorenali, Dipartimento di Medicina e Chirurgia, Università di Parma.

Università di Parma.

出版信息

Acta Biomed. 2021 Apr 30;92(S1):e2021162. doi: 10.23750/abm.v92iS1.9358.

Abstract

Background Fibromuscolar dysplasia (FMD) is an idiopathic, non-atherosclerotic and non-inflammatory stenotic lesion of renal arteries causing renovascular hypertension up-regulating renin-angiotensin-aldosterone system. Case report: A 18-year-old man was referred to our Hypertension Center (Clinica e Terapia Medica) for the recent onset of hypertension, poorly controlled on calcium channel blockers, already associated to electrocardiographic and echocardiography signs of left ventricular hypertrophy and significant albuminuria (728 mg/24 h). An increased plasma renin activity (PRA), aldosterone level and a mild hypokalemia raised the suspicion of renovascular hypertension. Abdominal CT and MRI angiography showed mild kidneys asymmetry and a tubular stenosis of the right renal artery in its mid-distal portion close to renal hilum. Radionuclide renal scintigraphy documented a kidneys asymmetry of separated glomerular filtration rate. Renal FMD was diagnosed based on patient age and the absence of cardiovascular risk factors for atherosclerosis. Patient successfully underwent right renal angioplasty giving a rapid normalization of blood pressure levels without antihypertensive drugs. Plasma aldosterone and PRA rapidly normalized as well as serum potassium levels. Six months after angioplasty echocardiography showed a regression of left ventricular hypertrophy and the patient albumin urine excretion became normal (14 mg/24 h). Conclusions FMD can cause renovascular hypertension associated to organ damage such myocardial hypertrophy and albuminuria through mechanisms dependent but also independent from blood pressure levels. Renal angioplasty turned off renin-angiotensin-aldosterone overactivity allowing the cure the hypertension and a surprisingly rapid reverse of myocardial hypertrophy and of excess of albumin urine excretion not only dependent on blood pressure normalization.

摘要

背景

纤维肌性发育不良(FMD)是一种特发性、非动脉粥样硬化和非炎症性的肾动脉狭窄病变,导致肾血管性高血压,上调肾素-血管紧张素-醛固酮系统。

病例报告

一名 18 岁男性因近期发生的高血压而被转诊至我们的高血压中心(Clinica e Terapia Medica)就诊,其高血压控制不佳,尽管已使用钙通道阻滞剂,但仍存在心电图和超声心动图左心室肥厚和大量白蛋白尿(728mg/24h)的迹象。血浆肾素活性(PRA)、醛固酮水平升高和轻度低钾血症提示肾血管性高血压。腹部 CT 和 MRI 血管造影显示双侧肾脏轻度不对称,右肾动脉中段至肾门附近呈管状狭窄。放射性核素肾闪烁显像证实了肾小球滤过率的肾脏不对称性。基于患者年龄和无动脉粥样硬化心血管危险因素,诊断为肾 FMD。患者成功接受了右肾血管成形术,血压水平迅速恢复正常,无需使用降压药物。血浆醛固酮和 PRA 以及血清钾水平迅速恢复正常。血管成形术后 6 个月,超声心动图显示左心室肥厚有所改善,患者的白蛋白尿排泄恢复正常(14mg/24h)。

结论

FMD 可引起肾血管性高血压,伴有心肌肥厚和白蛋白尿等器官损害,其机制既依赖于血压水平,也独立于血压水平。肾血管成形术阻断了肾素-血管紧张素-醛固酮的过度活跃,不仅依赖于血压的正常化,还可以治愈高血压,以及心肌肥厚和白蛋白尿过量的快速逆转。

https://cdn.ncbi.nlm.nih.gov/pmc/blobs/e503/8142778/952260108579/ACTA-92-162-g001.jpg

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