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四十余年来一个常染色体显性遗传假性醛固酮减少症家系中肾素-血管紧张素-醛固酮系统的评估:由于 NR3C2 基因突变所致。

Renin-aldosterone system evaluation over four decades in an extended family with autosomal dominant pseudohypoaldosteronism due to a deletion in the NR3C2 gene.

机构信息

Division of Pediatric Endocrinology, E. Wolfson Medical Center, Holon, Israel; Sackler School of Medicine, Tel-Aviv University, Tel Aviv, Israel.

Assistance Publique-Hôpitaux de Paris, Hôpital Européen Georges Pompidou, Service de Génétique, Paris, France; Centre de Références de Maladies Rénales Rares de l'Enfant et d'Adulte (MARHEA).

出版信息

J Steroid Biochem Mol Biol. 2020 Nov;204:105755. doi: 10.1016/j.jsbmb.2020.105755. Epub 2020 Oct 2.

Abstract

Renal pseudohypoaldosteronism (PHA1) is a mild form of an aldosterone-resistance syndrome caused by mutations in the NR3C2 gene that codes for the mineralocorticoid receptor (MR). The disease is inherited as an autosomal dominant trait characterized by signs and symptoms of salt-losing in infancy. Disease manifestations could be severe in infancy but improve after the age of 1-3 years. Some affected members are asymptomatic and remain so life-long. In this study, we report the identification of a large deletion in the NR3C2 gene (c.1897+1_1898-1)_(c.*2955+?)del in renal PHA1 patients from an extended family spanning four generations. We prospectively evaluated the plasma renin activity and serum aldosterone profiles over four decades in symptomatic and asymptomatic affected family members. The benefits of early diagnosis on the clinical outcome were assessed as well. The long-term follow-up showed an age-dependent decrease in both plasma renin activity and serum aldosterone levels over the years. However, aldosterone levels remain high life-long. Thus, levels of aldosterone are a reliable marker to detect asymptomatic family members. The diagnosis of the proposita led to early diagnosis and therapy in other affected family members, significantly mitigating the clinical course. Despite the extremely elevated serum aldosterone levels during pregnancy, affected pregnant women did not experience any ill effects. However, this should be verified by observations in other adult patients.

摘要

肾假性醛固酮减少症(PHA1)是一种由编码醛固酮受体(MR)的 NR3C2 基因突变引起的醛固酮抵抗综合征的轻度形式。这种疾病作为常染色体显性遗传特征,在婴儿期表现为失盐症状和体征。疾病表现可能在婴儿期严重,但在 1-3 岁后会改善。一些受影响的成员无症状,并终身保持无症状。在这项研究中,我们报道了在跨越四代的一个大家庭中,PHA1 患者的 NR3C2 基因(c.1897+1_1898-1)(c.*2955+?)del 发生大片段缺失。我们前瞻性地评估了 40 多年来有症状和无症状受影响家庭成员的血浆肾素活性和血清醛固酮谱。还评估了早期诊断对临床结果的益处。长期随访显示,血浆肾素活性和血清醛固酮水平随年龄呈依赖性降低。然而,醛固酮水平终生保持较高水平。因此,醛固酮水平是检测无症状家庭成员的可靠标志物。先证者的诊断导致了其他受影响家庭成员的早期诊断和治疗,显著改善了临床病程。尽管妊娠期间血清醛固酮水平极高,但受影响的孕妇没有任何不良影响。然而,这应该通过对其他成年患者的观察来验证。

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