Non-neoplastic/hyperplastic primary aldosteronism – Its histopathology and genotype

Yuto Yamazaki, Kei Omata, Yuta Tezuka, Xin Gao, Hiroko Ogata, Jacopo Pieroni, Yoshikiyo Ono, Ryo Morimoto, Yasuhiro Nakamura, Celso E. Gomez-Sanchez, Fumitoshi Satoh, Hironobu Sasano

Research output: Contribution to journalReview articlepeer-review

5 Citations (Scopus)


Recent development of genetic analysis has revealed the molecular characteristics of aldosterone-producing adrenocortical lesions, including gene mutations of KCNJ5, ATP1A1, ATP2B3, CACNA1D, CACNA1H, CTNNB1, and CLCN2. In addition, CYP11B2-based immunohistochemical analysis has made it possible to classify non-neoplastic lesions of primary aldosteronism (PA) into two distinct histological subtypes based on the localization of aldosterone-producing cells: multiple adrenocortical micronodules (MN) and diffuse hyperplasia of zona glomerulosa (DH). Among MNs, CACNA1D somatic mutation was most frequently detected in 60–80% of micronodules. The number and size of those CYP11B2-positive cell clusters/micronodules could therefore contribute to the pathogenesis or development of hyperaldosteronism. In addition, this newly developed histology- and genetics-based classification of non-neoplastic PA lesions have enabled the precise identification of the responsible lesions of aldosterone excess and enormous improvement of postoperative clinical management of patients with adrenocortical disorders.

Original languageEnglish
Pages (from-to)122-131
Number of pages10
JournalCurrent Opinion in Endocrine and Metabolic Research
Publication statusPublished - 2019 Oct


  • CYP11B2
  • Hyperplasia
  • Immunohistochemistry
  • KCNJ5
  • Next-generation sequencing (NGS)
  • Primary aldosteronism


Dive into the research topics of 'Non-neoplastic/hyperplastic primary aldosteronism – Its histopathology and genotype'. Together they form a unique fingerprint.

Cite this