TY - JOUR
T1 - Renal Injuries in Primary Aldosteronism
T2 - Quantitative Histopathological Analysis of 19 Patients with Primary Adosteronism
AU - Ogata, Hiroko
AU - Yamazaki, Yuto
AU - Tezuka, Yuta
AU - Gao, Xin
AU - Omata, Kei
AU - Ono, Yoshikiyo
AU - Kawasaki, Yoshihide
AU - Tanaka, Tomoaki
AU - Nagano, Hidekazu
AU - Wada, Norio
AU - Oki, Yutaka
AU - Ikeya, Akira
AU - Oki, Kenji
AU - Takeda, Yoshiyu
AU - Kometani, Mitsuhiro
AU - Kageyama, Kazunori
AU - Terui, Ken
AU - Gomez-Sanchez, Celso E.
AU - Liu, Shujun
AU - Morimoto, Ryo
AU - Joh, Kensuke
AU - Sato, Hiroshi
AU - Miyazaki, Mariko
AU - Ito, Akihiro
AU - Arai, Yoichi
AU - Nakamura, Yasuhiro
AU - Ito, Sadayoshi
AU - Satoh, Fumitoshi
AU - Sasano, Hironobu
N1 - Funding Information:
This work was supported by Japan Society for the Promotion of Science Grants-in-Aid for Scientific Research No. JP15H04711.
Funding Information:
H. Ogata is supported by a scholarship from the Takeda Science Foundation. We thank Mr Katsuhiko Ono for the preparation of the sections of biopsy specimens and Ms Kiyomi Kisu for the preparation of the sections of electron microscopy.
Publisher Copyright:
© 2021 Lippincott Williams and Wilkins. All rights reserved.
PY - 2021/8/1
Y1 - 2021/8/1
N2 - The rapid progression of chronic kidney disease and higher incidence of cardiovascular complications are well known in patients with hyperaldosteronism. However, detailed renal histopathologic characteristics of this disease have remained unknown. Therefore, renal biopsy specimens of 19 cases with unilateral hyperaldosteronism were compared with 22 autopsy renal cases of estimated glomerular filtration rate-matched essential hypertension without nephropathy or endocrine disorders to explore the hyperaldosteronism-specific histopathologic renal changes in this study. Global and segmental glomerulosclerosis, interstitial fibrosis, infiltration of inflammatory cells, arteriosclerosis, hyalinization of arterioles and immunoreactivity of mineralocorticoid receptor, 11β-hydroxysteroid dehydrogenase type 1 and 2, and renin were all quantitatively evaluated. The ultrastructural analysis was added in 3 hyperaldosteronism cases. Both mineralocorticoid receptor (P<0.01) and 11β-hydroxysteroid dehydrogenase type 2 (P<0.01) were significantly higher in renal tubules of hyperaldosteronism, which could result in enhancement of in situ aldosterone effects in hyperaldosteronism kidneys. Interstitial fibrosis was significantly more marked in hyperaldosteronism (P<0.01). The proportion of segmental glomerulosclerosis was also significantly higher in hyperaldosteronism (P<0.01). There were no significant differences of global glomerulosclerosis between 2 groups (P=0.08). Glomerular size was significantly larger in hyperaldosteronism (P<0.01). In medium size artery, luminal stenosis tended to be more marked (P=0.08), and intima-To-media ratio was significantly lower (P=0.02) in hyperaldosteronism. Arteriolar hyalinization was significantly more pronounced (P<0.01), especially at efferent arterioles (P<0.01) in hyperaldosteronism. Results above demonstrated more pronounced whole renal damages in hyperaldosteronism. Results of our present study also indicated the potential clinical significance of early intervention using mineralocorticoid receptor antagonists or blockers.
AB - The rapid progression of chronic kidney disease and higher incidence of cardiovascular complications are well known in patients with hyperaldosteronism. However, detailed renal histopathologic characteristics of this disease have remained unknown. Therefore, renal biopsy specimens of 19 cases with unilateral hyperaldosteronism were compared with 22 autopsy renal cases of estimated glomerular filtration rate-matched essential hypertension without nephropathy or endocrine disorders to explore the hyperaldosteronism-specific histopathologic renal changes in this study. Global and segmental glomerulosclerosis, interstitial fibrosis, infiltration of inflammatory cells, arteriosclerosis, hyalinization of arterioles and immunoreactivity of mineralocorticoid receptor, 11β-hydroxysteroid dehydrogenase type 1 and 2, and renin were all quantitatively evaluated. The ultrastructural analysis was added in 3 hyperaldosteronism cases. Both mineralocorticoid receptor (P<0.01) and 11β-hydroxysteroid dehydrogenase type 2 (P<0.01) were significantly higher in renal tubules of hyperaldosteronism, which could result in enhancement of in situ aldosterone effects in hyperaldosteronism kidneys. Interstitial fibrosis was significantly more marked in hyperaldosteronism (P<0.01). The proportion of segmental glomerulosclerosis was also significantly higher in hyperaldosteronism (P<0.01). There were no significant differences of global glomerulosclerosis between 2 groups (P=0.08). Glomerular size was significantly larger in hyperaldosteronism (P<0.01). In medium size artery, luminal stenosis tended to be more marked (P=0.08), and intima-To-media ratio was significantly lower (P=0.02) in hyperaldosteronism. Arteriolar hyalinization was significantly more pronounced (P<0.01), especially at efferent arterioles (P<0.01) in hyperaldosteronism. Results above demonstrated more pronounced whole renal damages in hyperaldosteronism. Results of our present study also indicated the potential clinical significance of early intervention using mineralocorticoid receptor antagonists or blockers.
KW - 11βHSD
KW - aldosterone
KW - histopathology
KW - hypertension
KW - mineralocorticoid receptor
KW - renin
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UR - http://www.scopus.com/inward/citedby.url?scp=85109479630&partnerID=8YFLogxK
U2 - 10.1161/HYPERTENSIONAHA.121.17436
DO - 10.1161/HYPERTENSIONAHA.121.17436
M3 - Article
C2 - 34120452
AN - SCOPUS:85109479630
VL - 78
SP - 411
EP - 421
JO - Hypertension
JF - Hypertension
SN - 0194-911X
IS - 2
ER -