Fernandes-Rosa Fábio L, Antonini Sonir R R
Departamento de Puericultura e Pediatria, Faculdade de Medicina de Ribeirão Preto, Universidade de São Paulo, SP.
Arq Bras Endocrinol Metabol. 2007 Apr;51(3):373-81. doi: 10.1590/s0004-27302007000300004.
Pseudohypoaldosteronism type 1 (PHA1) is a rare genetic disease characterized by neonatal renal salt wasting, vomiting, dehydration and failure to thrive. Affected patients present hyponatremia, hyperkalemia, associated with high levels of plasma renin and aldosterone resulting from a renal or systemic resistance to aldosterone. The systemic form of PHA1 results in a severe phenotype, and high doses of salt supplementation are necessary. The symptoms are life-long recurrent. This form is associated with autosomal recessive transmission. Homozygous or compound heterozygous loss of function mutations in the genes coding for the epithelial sodium channel (ENaC) subunities are responsible for this disease. The renal form of PHA1 results in a mild phenotype. Low doses of salt supplementation are required and usually the symptoms remit at the end of the first year of life. Heterozygous loss-of-function mutations in the mineralocorticoid receptor (MR) gene are associated with the renal form of PHA1 in the majority of the affected families but sporadic cases have been reported. In this review the mechanisms of aldosterone action and its effects are discussed. Additionally, clinical and molecular findings of a Brazilian family with the renal form of PHA1 caused by a nonsense mutation (R947X) in the MR gene are presented.
1型假性醛固酮增多症(PHA1)是一种罕见的遗传性疾病,其特征为新生儿肾性失盐、呕吐、脱水和发育不良。患病患者出现低钠血症、高钾血症,同时由于肾脏或全身对醛固酮产生抵抗,导致血浆肾素和醛固酮水平升高。PHA1的全身型会导致严重的表型,需要高剂量补充盐分。症状会终身反复出现。这种类型与常染色体隐性遗传有关。编码上皮钠通道(ENaC)亚基的基因发生纯合或复合杂合功能丧失突变是导致该疾病的原因。PHA1的肾脏型会导致轻度表型。需要低剂量补充盐分,症状通常在出生后第一年年底缓解。盐皮质激素受体(MR)基因杂合功能丧失突变在大多数患病家族中与PHA1的肾脏型有关,但也有散发病例的报道。在这篇综述中,讨论了醛固酮的作用机制及其影响。此外,还介绍了一个巴西家庭的临床和分子研究结果,该家庭的PHA1肾脏型由MR基因中的一个无义突变(R947X)引起。