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[Primary aldosteronism : Genetics and pathology].

U Scholl1,2

  • 1Medizinische Klinik mit Schwerpunkt Nephrologie und Internistische Intensivmedizin, Charité - Universitätsmedizin Berlin, Augustenburger Platz 1, 13353, Berlin, Deutschland. ute.scholl@charite.de.

Der Pathologe
|November 10, 2019
PubMed
Summary
This summary is machine-generated.

Genetic mutations are a key cause of primary aldosteronism, a common form of secondary hypertension. This review highlights somatic mutations in genes like KCNJ5, CACNA1D, ATP1A1, and ATP2B3, and familial forms involving other genes.

Keywords:
Aldosterone-producing adenomaAldosterone-producing cell clustersBilateral adrenal hyperplasiaIdiopathic hyperaldosteronismMutations

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Area of Science:

  • Endocrinology
  • Genetics
  • Hypertension Research

Background:

  • Primary aldosteronism (PA) is the most frequent cause of secondary hypertension.
  • It involves excessive aldosterone production, with common forms including bilateral adrenal hyperplasia and aldosterone-producing adenomas.

Purpose of the Study:

  • To review and synthesize key publications concerning the genetic underpinnings of primary aldosteronism.

Main Methods:

  • Literature review of publications on the genetic basis of primary aldosteronism.

Main Results:

  • Somatic mutations in KCNJ5, CACNA1D, ATP1A1, and ATP2B3 genes are identified causes of aldosterone-producing adenomas, leading to increased aldosterone.
  • Aldosterone-producing cell clusters, often with CACNA1D mutations, are implicated in bilateral hyperplasia.
  • Rare familial PA cases exhibit mutations in CYP11B2, CLCN2, KCNJ5, CACNA1H, or CACNA1D.

Conclusions:

  • A substantial proportion of primary aldosteronism cases result from somatic mutations in specific genes.
  • Further research is needed to explain correlations between mutations and clinical/histologic characteristics.